313 products
EUR-C001
Olaparib
Olaparib is a first-in-class oral PARP-1/2 inhibitor that exploits synthetic lethality in BRCA1/2-deficient tumours. By trapping PARP-protein complexes at DNA single-strand breaks, it prevents base-excision repair and drives replication fork collapse. FDA-approved for HER2-negative breast, ovarian, …
PARP1/PARP2
PARP-1/2 Inhibitor
≥99%
C24H23FN4O3
EUR-C002
Niraparib
Niraparib is a selective oral PARP-1/2 inhibitor with a distinct indazole carboxamide scaffold. Unlike olaparib, it does not require BRCA mutation for activity, showing efficacy in HRD-positive tumours regardless of BRCA status. Approved as maintenance therapy in platinum-sensitive recurrent ovarian…
PARP1/PARP2
PARP-1/2 Inhibitor
≥99%
C19H20N4O
EUR-C003
Rucaparib
Rucaparib is a tricyclic indole PARP-1/2/3 inhibitor that also inhibits PARP-associated activity including tankyrases. It traps PARP-DNA complexes with high potency and shows activity in BRCA-mutated and BRCA-wild-type HRD tumours. FDA-approved for BRCA1/2-mutated advanced ovarian and prostate cance…
PARP1/PARP2
PARP-1/2/3 Inhibitor
≥99%
C19H18FN3O
EUR-C004
Talazoparib
Talazoparib is the most potent clinical PARP trapper, with PARP trapping activity up to 100-fold greater than olaparib at equivalent concentrations. Its fluorinated pyrrolocarbazole scaffold confers exceptional DNA damage, making it highly effective in BRCA1/2-deficient cancer models. Approved for H…
PARP1/PARP2
PARP-1/2 Inhibitor
≥99%
C16H14F2N6O
EUR-C005
Sotorasib
Sotorasib is the first-approved KRAS G12C covalent inhibitor, binding irreversibly to the mutant cysteine 12 via an acrylamide warhead and locking KRAS in its GDP-bound inactive state. It selectively inhibits KRAS G12C without affecting wild-type KRAS or other RAS isoforms. FDA-approved for NSCLC wi…
KRAS
KRAS G12C Covalent Inhibitor
≥99%
C29H25F2N5O3
EUR-C006
Adagrasib
Adagrasib is a second-generation irreversible KRAS G12C inhibitor with an extended half-life (~23 h) enabling once-daily dosing and enhanced CNS penetration. Its dihydropyridopyrimidine scaffold provides improved pharmacokinetics versus sotorasib. FDA-approved for KRAS G12C-mutated NSCLC and CRC; sh…
KRAS
KRAS G12C Covalent Inhibitor
≥99%
C32H35F2N7O2
EUR-C007
Olomorasib
Olomorasib (LY3537982) is a next-generation KRAS G12C inhibitor with sub-nanomolar potency and differentiated binding kinetics. It demonstrates superior KRAS occupancy and sustained tumour suppression in preclinical models. Phase II/III trials are evaluating it in NSCLC, CRC, and other KRAS G12C-pos…
KRAS
KRAS G12C Covalent Inhibitor
≥99%
C29H29F2N5O3
EUR-C008
Garsorasib
Garsorasib (D-1553) is an oral, selective, irreversible KRAS G12C inhibitor with demonstrated intracranial efficacy in preclinical models, suggesting CNS penetration benefit. It exploits the GDP-binding pocket of mutant KRAS with high selectivity over wild-type RAS. Clinical data from the D-KRYSTAL …
KRAS
KRAS G12C Covalent Inhibitor
≥99%
C28H27F2N5O3
EUR-C009
Zoldonrasib
Zoldonrasib (RMC-9805) is a first-in-class tri-complex covalent KRAS G12D inhibitor from Revolution Medicines, exploiting cyclophilin A (CYPA) as a molecular glue to selectively inhibit KRAS G12D(ON). KRAS G12D is the most common KRAS mutation across pancreatic, colorectal, and lung cancers. Early P…
KRAS
KRAS G12D Covalent Inhibitor
≥99%
–
EUR-C013
Encorafenib
Encorafenib is a next-generation ATP-competitive BRAF inhibitor with an unusually long target residence time (>30 h), minimising paradoxical MAPK activation compared to earlier-generation agents. It selectively inhibits BRAF V600E/K/D mutants. FDA-approved in combination with binimetinib for BRAF V6…
BRAF
BRAF V600E/K Inhibitor
≥99%
C22H27ClFN7O4S
EUR-C014
Vepdegestrant
Vepdegestrant (ARV-471) is a first-in-class oral PROTAC that recruits the E3 ligase cereblon to selectively ubiquitinate and degrade estrogen receptor alpha (ERalpha). Unlike SERDs, it achieves near-complete ERalpha degradation including ESR1-mutant forms driving resistance to endocrine therapies. I…
ERalpha PROTAC Degrader
≥99%
C36H43F2N5O8S
EUR-C017
Relacorilant
Relacorilant is a selective, non-steroidal glucocorticoid receptor (GR) modulator lacking the anti-progesterone activity of mifepristone. It blocks cortisol-driven GR signalling without affecting mineralocorticoid or progesterone receptors. FDA-approved for cortisol-secreting adrenocortical carcinom…
Glucocorticoid Receptor (GR) Antagonist
≥99%
C29H29F4N3O4S
EUR-C018
Pirtobrutinib
Pirtobrutinib is the first approved non-covalent BTK inhibitor, binding reversibly to the BTK active site and maintaining potent inhibition regardless of C481 mutations that confer resistance to ibrutinib and acalabrutinib. Its kinase selectivity profile is highly focused on BTK. FDA-approved for re…
BTK
Non-Covalent (Reversible) BTK Inhibitor
≥99%
C28H29FN6O2
EUR-C019
Zongertinib
Zongertinib is a highly selective, covalent HER2 kinase inhibitor designed to spare EGFR, thereby reducing the diarrhoea and rash toxicities common to pan-ERBB inhibitors. It targets HER2 exon 20 insertions and other activating HER2 mutations. Approved for HER2-mutant (non-amplified) NSCLC based on …
HER2
HER2-Selective Tyrosine Kinase Inhibitor
≥99%
C21H22ClFN4O3
EUR-C020
Binimetinib
Binimetinib is an ATP-non-competitive allosteric MEK1/2 inhibitor with a halogenated benzimidazole scaffold. It blocks ERK phosphorylation downstream of BRAF/RAS, suppressing MAPK pathway proliferative signalling. FDA-approved in combination with encorafenib for BRAF V600E/K-mutant unresectable or m…
MEK1/MEK2
MEK1/2 Inhibitor
≥99%
C17H15BrF2N4O3
EUR-C021
Cobimetinib
Cobimetinib is a highly selective ATP-non-competitive MEK1/2 inhibitor. When combined with vemurafenib (BRAF V600E inhibitor), it provides more complete MAPK pathway suppression and delays acquired resistance. FDA-approved in combination with vemurafenib for BRAF V600E/K-mutant advanced melanoma. Re…
MEK1/MEK2
MEK1/2 Inhibitor
≥99%
C21H21F3IN3O2
EUR-C022
Mirdametinib
Mirdametinib (PD-0325901) is a second-generation allosteric MEK1/2 inhibitor with improved oral bioavailability and longer duration of ERK inhibition versus CI-1040. It forms a covalent interaction with Cys121 in the MEK allosteric pocket. FDA-approved for neurofibromatosis type 1 (NF1)-associated p…
MEK1/MEK2
MEK1/2 Inhibitor
≥99%
C16H14BrF2N2O3
EUR-C023
Selumetinib
Selumetinib is an orally bioavailable MEK1/2 inhibitor approved for paediatric NF1-associated symptomatic, inoperable plexiform neurofibromas. It selectively blocks MEK1/2 without requiring direct RAS interaction, making it active across multiple RAS-mutant contexts. Preclinical and clinical studies…
MEK1/MEK2
MEK1/2 Inhibitor
≥99%
C17H15BrClFN4O3
EUR-C024
Ulixertinib
Ulixertinib (BVD-523) is a reversible, ATP-competitive ERK1/2 inhibitor that targets the MAPK pathway downstream of MEK, overcoming common upstream resistance mechanisms to BRAF and MEK inhibitors. It inhibits ERK1/2 phosphorylation of RSK and other substrates. In clinical trials across MAPK-driven …
ERK1/2 Inhibitor
≥99%
C24H22ClFN4O3
EUR-C025
Dabrafenib
Dabrafenib is an ATP-competitive BRAF inhibitor selective for V600E/K/D mutant isoforms, bearing a fluorinated difluorophenylsulfonamide scaffold. When combined with trametinib (MEK inhibitor), it provides vertical MAPK pathway blockade. FDA-approved in combination with trametinib for BRAF V600-muta…
BRAF
BRAF V600E/K/D Inhibitor
≥99%
C23H20F3N5O2S2
EUR-C026
Vemurafenib
Vemurafenib was the first-in-class BRAF V600E inhibitor approved in oncology, demonstrating landmark efficacy in metastatic melanoma. It occupies the ATP-binding pocket via a sulfonamide pharmacophore. Paradoxical RAF dimerisation-driven MAPK reactivation limits durability; combination with MEK inhi…
BRAF
BRAF V600E Inhibitor
≥99%
C23H18ClF2N3O3S
EUR-C027
Alpelisib
Alpelisib is the first approved PI3Kalpha-selective inhibitor (Class I PI3K, p110alpha isoform), specifically targeting PIK3CA-mutant tumours. Its isoform selectivity reduces metabolic toxicity versus pan-PI3K inhibitors. FDA-approved in combination with fulvestrant for HR+/HER2- PIK3CA-mutated adva…
PI3K
PI3Kalpha-Selective Inhibitor
≥99%
C19H22FN5O2S
EUR-C028
Capivasertib
Capivasertib is an ATP-competitive, orally bioavailable pan-AKT inhibitor that blocks all three AKT isoforms with comparable potency. It is active against PIK3CA, AKT1, and PTEN-altered tumours—the main activating lesions of the PI3K pathway. FDA-approved in combination with fulvestrant for HR+/HER2…
AKT
Pan-AKT (AKT1/2/3) Inhibitor
≥99%
C22H22Cl2N4O2
EUR-C029
Inavolisib
Inavolisib is a next-generation PI3Kalpha-selective inhibitor with a distinct mechanism that also promotes degradation of mutant p110alpha protein, providing dual inhibitory and degrader activity. Unlike alpelisib, it shows reduced hyperglycaemia in preclinical studies. FDA-approved in combination w…
PI3K
PI3Kalpha-Selective Inhibitor / degrader activity
≥99%
C20H19FN6O3
EUR-C030
Ipatasertib
Ipatasertib is an oral, highly selective pan-AKT inhibitor with a distinct chromenone scaffold developed by Genentech/Roche. It inhibits AKT1/2/3 with IC50 values in the low nanomolar range and shows particular activity in PTEN-deficient and PIK3CA-mutant models. Phase III trials (IPATunity130/150) …
AKT
Pan-AKT (AKT1/2/3) Inhibitor
≥99%
C25H26FN5O3
EUR-C031
Pictilisib
Pictilisib (GDC-0941) is a potent, selective pan-PI3K inhibitor targeting all Class I isoforms (p110alpha/beta/delta/gamma) with low nanomolar potency. It competitively inhibits ATP binding in the PI3K catalytic domain and suppresses downstream AKT and S6K phosphorylation. Used extensively as a rese…
Pan-PI3K Inhibitor (Class I)
≥99%
C23H26N6O3S
EUR-C032
Sapanisertib
Sapanisertib (INK128/MLN0128) is a highly selective ATP-competitive mTOR inhibitor that blocks both mTORC1 and mTORC2, overcoming the AKT feedback reactivation seen with allosteric mTORC1-only inhibitors like rapamycin. It achieves more complete 4E-BP1 and S6K inhibition. Multiple Phase I/II trials …
mTOR
mTORC1/2 Dual Inhibitor
≥99%
C16H16N8O
EUR-C033
Wortmannin
Wortmannin is a steroidal fungal metabolite and irreversible PI3K inhibitor that covalently modifies Lys802 in the PI3K ATP-binding site. It also inhibits related kinases including DNA-PK and mTOR at higher concentrations, making it a broad PI3K/PIKK research tool. While too toxic for clinical use, …
PI3K
PI3K Inhibitor (irreversible) / DNA-PK Inhibitor
≥99%
C19H18O8
EUR-C034
Abemaciclib
Abemaciclib is a potent CDK4/6 inhibitor with ~14-fold selectivity for CDK4 over CDK6 and the unique ability to be given continuously due to its improved tolerability profile. It causes G1 cell cycle arrest by preventing Rb phosphorylation. FDA-approved as monotherapy and in combination with endocri…
CDK4/CDK6
CDK4/6 Inhibitor
≥99%
C27H32F2N8
EUR-C035
Dinaciclib
Dinaciclib is a potent pan-CDK inhibitor with sub-nanomolar activity against CDK1, 2, 5, and 9. Unlike selective CDK4/6 inhibitors, it induces apoptosis rather than cytostasis by disrupting both cell cycle progression and transcriptional elongation (via CDK9/P-TEFb). Extensively studied in preclinic…
CDK1/2/5/9 Inhibitor
≥99%
C20H28N6O2
EUR-C036
Palbociclib
Palbociclib was the first approved CDK4/6 inhibitor, fundamentally changing the standard of care for HR+/HER2- advanced breast cancer. It selectively inhibits CDK4 and CDK6, arresting cells in G1 by preventing Rb hyperphosphorylation. The HCl salt provides improved aqueous solubility for research ap…
CDK4/CDK6
CDK4/6 Inhibitor
≥99%
C24H29N7O2 · HCl
EUR-C037
Ribociclib
Ribociclib is a CDK4/6 inhibitor with demonstrated overall survival benefit across multiple Phase III trials (MONALEESA-2/3/7), making it one of the few targeted agents with confirmed OS improvement in HR+/HER2- breast cancer. Its pyrido[3,4-d]pyrimidine core provides tight CDK4/6 binding. QTc prolo…
CDK4/CDK6
CDK4/6 Inhibitor
≥99%
C23H30N8O
EUR-C038
Afatinib
Afatinib is a second-generation irreversible pan-ERBB inhibitor that covalently modifies Cys797 on EGFR, Cys805 on HER2, and Cys803 on HER4 via an acrylamide warhead. It overcomes T790M-independent resistance to first-generation EGFR TKIs and is active against EGFR exon 19 deletions and L858R mutati…
EGFRHER2
Pan-ERBB (EGFR/HER2/HER4) Covalent Inhibitor
≥99%
C24H25ClFN5O3
EUR-C039
Neratinib
Neratinib is an irreversible pan-ERBB kinase inhibitor with covalent binding to conserved cysteines across EGFR, HER2, and HER4. It is uniquely active against HER2 exon 20 insertions, which are insensitive to most other EGFR/HER2 inhibitors. FDA-approved as extended adjuvant therapy in HER2-positive…
EGFRHER2
Pan-ERBB (EGFR/HER2/HER4) Covalent Inhibitor
≥99%
C30H29ClN4O3
EUR-C040
Osimertinib
Osimertinib is the global standard-of-care third-generation EGFR TKI that covalently inhibits both sensitising mutations (exon 19 del, L858R) and the T790M resistance gatekeeper mutation. Its indole acrylamide warhead forms a covalent bond with Cys797, and CNS penetration is superior to earlier-gene…
EGFR
3rd-Generation EGFR TKI (T790M + exon 19/21)
≥99%
C28H33N7O2
EUR-C041
Tucatinib
Tucatinib is a highly selective, reversible HER2 kinase inhibitor with >1000-fold selectivity over EGFR, minimising EGFR-related toxicities. It is CNS-penetrant and demonstrates intracranial activity in HER2+ brain metastases. FDA-approved in combination with trastuzumab and capecitabine for HER2+ m…
HER2
HER2-Selective TKI
≥99%
C26H24FN7O2
EUR-C042
Ceritinib
Ceritinib is a second-generation ATP-competitive ALK inhibitor ~20-fold more potent than crizotinib in biochemical assays, overcoming most crizotinib-acquired resistance mutations (L1196M, G1269A, I1171T). It also inhibits ROS1, IGF-1R, and insulin receptor. FDA-approved for ALK-positive, metastatic…
ALK
ALK/ROS1/IGF-1R/InsR Inhibitor
≥99%
C28H36ClN5O3S
EUR-C043
Entrectinib
Entrectinib is a CNS-penetrant, multi-kinase inhibitor targeting TRKA/B/C (NTRK1/2/3 fusions), ROS1 rearrangements, and ALK rearrangements with high potency. It was the first agent approved specifically for NTRK fusion-positive solid tumours regardless of histology (tumour-agnostic). FDA approved fo…
ALK
ALK/ROS1/TRK (TRKA/B/C) Inhibitor
≥99%
C31H29F2N5O2
EUR-C044
Lorlatinib
Lorlatinib is a third-generation macrocyclic ALK/ROS1 inhibitor specifically designed for CNS penetration and activity against compound ALK resistance mutations including G1202R. Its macrocyclic structure confers superior CNS penetration. FDA-approved as first-line and post-crizotinib therapy for AL…
ALK
3rd-Generation ALK/ROS1 Inhibitor
≥99%
C21H19FN4O2
EUR-C045
Erdafitinib
Erdafitinib is the first approved pan-FGFR inhibitor targeting FGFR1/2/3/4, with particular activity against FGFR3 mutations and FGFR2 fusions prevalent in urothelial cancer. It competitively inhibits FGFR ATP binding, suppressing FGFR-driven MAPK and PI3K/AKT signalling. FDA-approved for locally ad…
Pan-FGFR (FGFR1/2/3/4) Inhibitor
≥99%
C25H30N6O2
EUR-C046
Infigratinib
Infigratinib is an ATP-competitive FGFR1/2/3 inhibitor with relative selectivity over FGFR4, potentially reducing hepatotoxicity associated with FGFR4 inhibition. It was approved for previously treated, FGFR2 fusion/rearrangement-positive, locally advanced or metastatic cholangiocarcinoma. Activity …
FGFR1/2/3-Selective Inhibitor
≥99%
C23H27Cl2F2N5O3
EUR-C047
Capmatinib
Capmatinib is a potent, selective c-MET inhibitor with nanomolar activity against METex14-skipping mutations and high-level MET amplification. Its triazolo-quinoxaline scaffold provides tight ATP-competitive binding to the MET kinase domain. FDA-approved for adults with metastatic NSCLC harbouring M…
c-MET (METex14 / MET-amplified) Inhibitor
≥99%
C23H17FN6O
EUR-C048
Adavosertib
Adavosertib (MK-1775) is an ATP-competitive WEE1 kinase inhibitor that abrogates the G2/M DNA damage checkpoint by preventing inhibitory phosphorylation of CDK1 (Tyr15). This forces checkpoint-deficient cancer cells (commonly p53-mutant) into mitotic catastrophe following DNA damage. Extensively stu…
WEE1 Kinase Inhibitor
≥99%
C27H23FN8O2
EUR-C049
Alisertib
Alisertib is a selective Aurora Kinase A inhibitor that disrupts mitotic spindle assembly by preventing AURKA-mediated phosphorylation of TACC3 and other centrosomal substrates, leading to multipolar spindle formation and mitotic exit failure. Shows particular activity in MYC-amplified haematologica…
Aurora Kinase A (AURKA) Inhibitor
≥99%
C27H20ClFN4O4
EUR-C050
Berzosertib
Berzosertib (M6620) is a first-in-class selective ATR kinase inhibitor that abrogates replication stress responses by blocking ATR-mediated CHK1 activation. Cancer cells with elevated replication stress (RAS mutations, CCNE1 amplification, ATM loss) are particularly sensitised. In combination with D…
ATR Kinase Inhibitor
≥99%
C22H16N6O3
EUR-C051
Ceralasertib
Ceralasertib is an orally bioavailable ATR inhibitor with distinct pharmacokinetics from berzosertib. It induces replication catastrophe in ATM-deficient or replication stress-high tumours and synergises with PARP inhibitors, chemotherapy, and immunotherapy. Multiple clinical trials investigate it a…
ATR Kinase Inhibitor
≥99%
C20H21ClN6O3S
EUR-C052
Defactinib
Defactinib is an ATP-competitive FAK inhibitor that disrupts integrin-mediated cell survival signalling and tumour-stroma interactions. FAK inhibition reduces tumour-associated immunosuppression, depleting regulatory T cells and MDSCs in the tumour microenvironment. Particularly active in mesothelio…
Focal Adhesion Kinase (FAK) Inhibitor
≥99%
C24H23F3N6O3S
EUR-C053
Nedisertib
Nedisertib (peposertib) is a potent, selective DNA-dependent protein kinase (DNA-PKcs) inhibitor that blocks NHEJ-mediated repair of ionising radiation-induced double-strand breaks. By sensitising tumour cells to radiation, it provides a rational combination partner in radiotherapy. Clinical studies…
DNA-PK (DNA-PKcs) Inhibitor
≥99%
C26H22N6O2
EUR-C054
Entinostat
Entinostat is an oral Class I-selective HDAC inhibitor with a benzamide scaffold providing selectivity for HDAC1/2/3 over Class IIa/b enzymes. By restoring acetylation of histones and non-histone proteins, it induces re-expression of silenced tumour suppressors and modulates immune cell populations.…
Class I HDAC (HDAC1/2/3) Inhibitor
≥99%
C21H20N4O3
EUR-C055
Decitabine
Decitabine (5-aza-2'-deoxycytidine) is a nucleoside analogue that incorporates into DNA and irreversibly traps DNA methyltransferases (DNMT1/3a/3b), causing passive demethylation of CpG islands and reactivating silenced tumour suppressor genes. FDA-approved for MDS; increasingly investigated in comb…
DNA Methyltransferase Inhibitor (DNMT1/3a/3b)
≥99%
C8H12N4O4
EUR-C056
Saruparib
Saruparib is a next-generation PARP1-selective inhibitor (~100-fold selectivity over PARP2) designed to maintain anti-tumour efficacy while reducing haematological toxicity associated with PARP1/2 dual inhibition. Enhanced PARP1 trapping potency relative to olaparib. Phase I/II data across BRCA1/2-m…
PARP1/PARP2
PARP1-Selective Inhibitor (next-generation PARP trapper)
≥99%
C21H24FN5O3S
EUR-C057
Axitinib
Axitinib is a potent, selective second-generation VEGFR1/2/3 inhibitor with substantially lower off-target kinase activity than sunitinib. It suppresses tumour angiogenesis by blocking VEGF-driven endothelial proliferation and survival. FDA-approved in combination with pembrolizumab or avelumab for …
EGFRVEGFR
VEGFR1/2/3 Inhibitor (2nd-Generation)
≥99%
C22H18N4OS
EUR-C058
Cabozantinib
Cabozantinib simultaneously inhibits VEGFR1/2/3, MET, AXL, RET, and KIT, addressing multiple escape mechanisms from single-target anti-angiogenics. AXL and MET co-inhibition reduces immunosuppression and epithelial-mesenchymal transition. FDA-approved for RCC (1st-line with nivolumab or monotherapy)…
EGFRVEGFR
Multi-target TKI: VEGFR/MET/AXL/RET Inhibitor
≥99%
C28H24FN3O5
EUR-C059
Lenvatinib
Lenvatinib is a multi-target receptor tyrosine kinase inhibitor with broad activity against VEGFR1-3, FGFR1-4, PDGFRalpha, RET, and KIT. FGFR co-inhibition differentiates it from most anti-VEGFR agents. FDA-approved as monotherapy for thyroid cancers and in combination with everolimus or pembrolizum…
EGFRVEGFR
Multi-target TKI: VEGFR/FGFR/PDGFR/RET/KIT Inhibitor
≥99%
C25H23ClN4O4
EUR-C060
Nintedanib
Nintedanib is an indolyl-carbamide triple angiokinase inhibitor targeting VEGFR1/2/3, PDGFR-alpha/beta, and FGFR1/2/3. In oncology, it is approved in combination with docetaxel for second-line NSCLC with adenocarcinoma histology. Its primary approval (Ofev) is for idiopathic pulmonary fibrosis; this…
EGFRVEGFR
Multi-target TKI: VEGFR/PDGFR/FGFR Inhibitor
≥99%
C31H33N3O4
EUR-C061
Regorafenib
Regorafenib is an oral multikinase inhibitor with a broad target spectrum including VEGFR1/2/3, TIE2, BRAF/CRAF, KIT, RET, PDGFRbeta, and FGFR1. It is active in late-line metastatic CRC, GIST, and HCC. The additional TIE2/angiopoietin pathway inhibition distinguishes it from sunitinib-class agents; …
EGFRBRAFVEGFR
Multi-target TKI: VEGFR/TIE2/BRAF/KIT/RET/PDGFR Inhibitor
≥99%
C21H15ClF4N4O3
EUR-C062
Semaxinib
Semaxinib (SU5416) is the first selective VEGFR2 inhibitor developed, demonstrating proof-of-concept for anti-angiogenic therapy in oncology research. It competitively inhibits VEGFR2/KDR ATP binding, suppressing VEGF-stimulated endothelial proliferation and tube formation in vitro. Now primarily us…
EGFRVEGFR
VEGFR2 (KDR/Flk-1) Inhibitor
≥99%
C12H11N2O · Na
EUR-C063
Acalabrutinib
Acalabrutinib is a second-generation, highly selective covalent BTK inhibitor with reduced off-target activity versus ibrutinib against ITK, EGFR, and TEC family kinases. Its propiolamide warhead forms an irreversible bond with BTK Cys481. FDA-approved for CLL/SLL and relapsed/refractory MCL; improv…
BTK
BTK Inhibitor (2nd-Gen | Covalent C481)
≥99%
C26H23N7O2
EUR-C064
Fedratinib
Fedratinib is a selective JAK2 inhibitor with additional FLT3 activity that retains activity in JAK2V617F-driven myeloproliferative neoplasms. Unlike ruxolitinib, it is active against mutant calreticulin (CALR)-driven MPNs. FDA-approved for intermediate-2 and high-risk myelofibrosis, including after…
JAK2/FLT3 Inhibitor
≥99%
C27H36N6O3S
EUR-C065
Gilteritinib
Gilteritinib is a potent, selective FLT3/AXL inhibitor active against both FLT3-ITD (internal tandem duplications) and FLT3-TKD (tyrosine kinase domain) mutations, including the D835 resistance mutation that limits quizartinib. AXL co-inhibition disrupts FLT3 inhibitor escape signalling. FDA-approve…
FLT3 (ITD/TKD) and AXL Inhibitor
≥99%
C29H38FN7O2
EUR-C066
Ibrutinib
Ibrutinib is the first-in-class irreversible BTK inhibitor, covalently modifying BTK Cys481 to block BCR-dependent B-cell survival and proliferation. Its broad kinase inhibition profile (ITK, TEC, EGFR, HER2) contributes to both activity and toxicity. FDA-approved for CLL, MCL, WM, MZL, and cGVHD; e…
BTK
BTK Inhibitor (1st-Gen | Covalent C481)
≥99%
C25H24N6O2
EUR-C067
Ivosidenib
Ivosidenib selectively inhibits mutant IDH1 (R132H/C/S/G/L) which produces the oncometabolite 2-hydroxyglutarate (2-HG), causing epigenetic dysregulation and impaired haematopoietic differentiation. By reducing 2-HG levels, it enables myeloid differentiation. FDA-approved for IDH1-mutant AML (frontl…
IDH1 (R132H/C/S/G/L) Mutant Inhibitor
≥99%
C28H22ClF3N6O3
EUR-C068
Quizartinib
Quizartinib is a highly potent, selective FLT3 inhibitor with sub-nanomolar activity against FLT3-ITD-positive AML. Unlike gilteritinib, it has limited activity against FLT3-TKD mutations (D835), which limits its utility in TKD-driven resistance. FDA-approved in combination with standard consolidati…
FLT3-ITD Selective Inhibitor
≥99%
C29H32FN5O4S
EUR-C069
Revumenib
Revumenib is a first-in-class small-molecule inhibitor that disrupts the protein-protein interaction between menin and KMT2A (MLL1), a critical oncogenic complex in KMT2A-rearranged and NPM1-mutant AML. By blocking this interaction, it reverses aberrant HOX/MEIS1 gene expression programmes. FDA-appr…
Menin-KMT2A (MLL1) Interaction Inhibitor
≥99%
C35H37Cl2FN6O3
EUR-C070
Tofacitinib
Tofacitinib is a first-in-class oral JAK inhibitor with preferential activity against JAK1/JAK3 over JAK2, suppressing signalling through the common gamma chain cytokine receptors (IL-2, IL-4, IL-7, IL-9, IL-15, IL-21). In oncology research it is used to block JAK/STAT3 signalling in cytokine-driven…
JAK1/JAK3 Inhibitor
≥99%
C16H20N6O
EUR-C071
Volasertib
Volasertib is a potent, selective PLK1 inhibitor that disrupts mitotic entry and causes mitotic arrest through spindle assembly checkpoint engagement. PLK1 is frequently overexpressed in AML and poor-prognosis solid tumours. Received FDA Breakthrough Therapy designation for AML in combination with l…
PLK1 (Polo-Like Kinase 1) Inhibitor
≥99%
C30H43N7O3
EUR-C072
Ponatinib
Ponatinib is a third-generation BCR-ABL1 inhibitor specifically engineered to inhibit the T315I gatekeeper mutation that confers resistance to all first- and second-generation TKIs. Its carbon-carbon triple bond pharmacophore avoids steric clash with the T315I methyl group. FDA-approved for CML and …
EGFRVEGFR
Pan-BCR-ABL1 / PDGFR / VEGFR / FGFR TKI
≥99%
C29H27FN6O
EUR-C073
Avasimibe
Avasimibe is a sulfonamide-based inhibitor of ACAT (acyl-CoA:cholesterol acyltransferase; SOAT1/2) that reduces intracellular cholesterol esterification. In oncology research, SOAT1/ACAT1 inhibition depletes free cholesterol in the ER, disrupting lipid raft signalling. Preclinical studies demonstrat…
ACAT (SOAT1/SOAT2) Inhibitor
≥99%
C26H33NO4S
EUR-C074
Belzutifan
Belzutifan is a first-in-class oral HIF-2alpha inhibitor that blocks the dimerisation of HIF-2alpha (EPAS1) with ARNT, preventing transcription of hypoxia-response genes including VEGF, EPO, and GLUT1. In VHL-deficient tumours, constitutive HIF-2alpha activity drives tumorigenesis. FDA-approved for …
HIF-2alpha (EPAS1) Inhibitor
≥99%
C20H14F3N3O2S
EUR-C075
Bemcentinib
Bemcentinib is a first-in-class selective AXL inhibitor that blocks Gas6-AXL signalling, a key driver of epithelial-mesenchymal transition, metastasis, and innate immune evasion. AXL overexpression correlates with resistance to EGFR, VEGFR, and checkpoint inhibitors. In clinical development for AML,…
AXL Receptor Tyrosine Kinase Inhibitor
≥99%
C29H35N5O2
EUR-C076
Brequinar
Brequinar is a quinolinecarboxylic acid derivative that potently inhibits DHODH, the rate-limiting enzyme in the de novo pyrimidine synthesis pathway. Cancer cells with high proliferative demand rely disproportionately on de novo pyrimidine synthesis. DHODH inhibition induces myeloid differentiation…
DHODH (Dihydroorotate Dehydrogenase) Inhibitor
≥99%
C23H15F2NO2
EUR-C077
Canagliflozin
Canagliflozin is an SGLT2 inhibitor approved for type 2 diabetes and cardio-renal protection. In oncology research, canagliflozin additionally inhibits mitochondrial complex I and activates AMPK at pharmacological concentrations, suppressing mTOR and PI3K-AKT signalling. Preclinical studies show ant…
SGLT2 (SLC5A2) Inhibitor
≥99%
C24H25FO5S
EUR-C078
Cilengitide
Cilengitide is a cyclic pentapeptide (cyclo-RGDfK) integrin inhibitor that selectively antagonises alphavbeta3 and alphavbeta5 integrins, disrupting tumour angiogenesis and invasion. It has both anti-angiogenic and direct anti-tumour effects through anoikis induction. Despite promising preclinical r…
alphavbeta3 / alphavbeta5 Integrin Inhibitor (cyclic RGD peptide)
≥99%
C27H34N8O7
EUR-C079
Enzalutamide
Enzalutamide is a next-generation androgen receptor antagonist that competitively inhibits AR with ~8-fold greater affinity than bicalutamide, and additionally blocks AR nuclear translocation and DNA binding. It remains active in cells with AR overexpression that convert bicalutamide into a partial …
Androgen Receptor (AR) Antagonist / Nuclear Import Inhibitor
≥99%
C21H16F4N4O2S
EUR-C080
Eribulin
Eribulin is a synthetic macrocyclic ketone analogue of halichondrin B, a natural product from the marine sponge Halichondria okadai. It binds specifically to the plus ends of microtubules, suppressing dynamic instability without affecting depolymerisation—a distinct mechanism from taxanes. FDA-appro…
Microtubule Dynamics Inhibitor (halichondrin analogue)
≥99%
C40H59NO11
EUR-C081
Galunisertib
Galunisertib is a selective, ATP-competitive ALK5 (TGF-betaRI) inhibitor that blocks TGF-beta-mediated SMAD2/3 phosphorylation, disrupting tumour immune evasion, angiogenesis, and stromal remodelling. TGF-beta is a master immunosuppressive cytokine in solid tumour microenvironments. Extensively stud…
ALK
TGF-betaR1 (ALK5) Inhibitor
≥99%
C18H14N4O
EUR-C082
Linsitinib
Linsitinib is an oral, ATP-competitive dual IGF-1R and insulin receptor (InsR) inhibitor, blocking ligand-stimulated receptor autophosphorylation and downstream IRS-1/PI3K/AKT signalling. IGF-1R co-inhibition with InsR prevents the compensatory hyperinsulinaemia-driven InsR activation that limits se…
IGF-1R / InsR Dual Inhibitor
≥99%
C20H17N5O
EUR-C083
Pexidartinib
Pexidartinib is a selective CSF1R inhibitor that depletes tumour-associated macrophages (TAMs) by blocking M-CSF signalling critical for monocyte-macrophage survival and differentiation. TAM depletion reduces immunosuppression and enhances T-cell infiltration. FDA-approved for adults with symptomati…
CSF1R / KIT / FLT3 Inhibitor
≥99%
C20H15ClF3N5
EUR-C084
Plicamycin
Plicamycin (mithramycin A) is a glycosylated aureolic acid antibiotic that intercalates into GC-rich DNA regions and displaces SP1/SP3 transcription factors, suppressing expression of SP1-driven oncogenes including c-MYC, MDM2, and telomerase. It is a potent calcium-lowering agent used clinically fo…
RNA Polymerase Inhibitor / GC-rich DNA Binder / SP1 Inhibitor
≥99%
C52H76O24
EUR-C085
Puromycin
Puromycin dihydrochloride is an aminonucleoside antibiotic that causes premature chain termination by mimicking aminoacyl-tRNA. In research, it is the standard selectable marker in lentiviral and retroviral vector systems expressing the puromycin N-acetyltransferase (pac) resistance gene. Provides r…
Protein Synthesis Inhibitor (aminonucleoside antibiotic)
≥99%
C22H29N7O5 · 2HCl
EUR-C086
Rolipram
Rolipram is a selective cAMP-specific PDE4 inhibitor that elevates intracellular cAMP by blocking its hydrolysis, modulating PKA/EPAC signalling. In oncology research, PDE4 inhibition has anti-inflammatory and pro-apoptotic effects in multiple myeloma and CLL, and synergises with HDAC inhibitors. Us…
PDE4 (Phosphodiesterase 4) Inhibitor
≥99%
C16H21NO3
EUR-C087
Saracatinib
Saracatinib is a potent ATP-competitive Src family kinase and Abl inhibitor. Src family kinases mediate integrin-dependent invasion, EGFR transactivation, and resistance to multiple targeted therapies. Saracatinib is actively investigated as a combination partner to overcome invasion-related resista…
Src / Abl Dual Kinase Inhibitor
≥99%
C28H32ClN5O5
EUR-C088
Silmitasertib
Silmitasertib is the first selective, orally available CK2 inhibitor to enter clinical trials. CK2 is a constitutively active serine/threonine kinase that phosphorylates over 300 substrates including PTEN, p21, and caspase-3, promoting survival and suppressing apoptosis. Active in haematological mal…
CK2 (Casein Kinase 2) Inhibitor
≥99%
C20H14ClN3O2
EUR-C089
Telaglenastat
Telaglenastat is a first-in-class, orally bioavailable glutaminase (GLS1) inhibitor that blocks the conversion of glutamine to glutamate, depleting TCA cycle intermediates and GSH in glutamine-addicted cancers. Tumours with MYC amplification, mTOR activation, or RAS mutations rely heavily on glutami…
Glutaminase (GLS1 / KGA) Inhibitor
≥99%
C26H22BrF2N5O4S
EUR-C090
Vismodegib
Vismodegib is the first FDA-approved Hedgehog (Hh) pathway inhibitor, binding allosterically to Smoothened (SMO) and blocking downstream GLI1/2 transcription factor activation. It is highly effective in basal cell carcinoma (BCC) driven by PTCH1 loss or SMO gain-of-function mutations. FDA-approved f…
Hedgehog Pathway / SMO Inhibitor
≥99%
C19H14Cl2N2O3
EUR-C091
Adezmapimod
Adezmapimod (SB203580) is a selective pyridinyl imidazole p38alpha/beta MAPK inhibitor that blocks stress-activated MAPK signalling, inflammatory cytokine production (TNF-alpha, IL-1beta), and MAPKAP-K2 phosphorylation. Used extensively as a research tool for dissecting stress-activated signalling p…
p38 MAPK (p38alpha/beta) Inhibitor
≥99%
C21H16FN3OS
EUR-C096
Raleukin
Raleukin is an engineered recombinant IL-2 analogue designed to preferentially engage the intermediate-affinity IL-2Rbeta-gamma receptor on effector T cells and NK cells while reducing binding to the high-affinity IL-2Ralpha (CD25) receptor on immunosuppressive regulatory T cells. This selectivity i…
IL-2 Receptor Agonist (recombinant IL-2 analogue)
≥95%
Recombinant human IL-2 (cytokine)
EUR-C101
Daraxonrasib
Daraxonrasib (RMC-6236) is a first-in-class non-covalent KRAS(ON) inhibitor that forms a tri-complex with cyclophilin A (CYPA) as a molecular glue, selectively inhibiting the active (GTP-bound) form of RAS across multiple oncogenic variants including KRAS G12D, G12V, G12C, G13D, and wild-type KRAS i…
Pan-RAS(ON) Multi-Selective Inhibitor (non-covalent tri-complex)
≥99%
C44H58N8O5S
EUR-C102
Mobocertinib
Mobocertinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
EGFR
EGFR Exon 20 Insertion-Selective TKI
≥98%
C39H48ClN7O4
EUR-C103
Tivozanib
Tivozanib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
EGFRVEGFR
Pan-VEGFR (VEGFR1/2/3) Inhibitor
≥98%
C22H19ClN4O5
EUR-C104
Tepotinib
Tepotinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
MET Inhibitor
≥98%
C29H28FN5O3
EUR-C105
Pralsetinib
Pralsetinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
RET Inhibitor
≥98%
C27H32FN7O2
EUR-C106
Pemigatinib
Pemigatinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
FGFR1/2/3 Selective Inhibitor
≥98%
C24H24F2N4O5S
EUR-C107
Ripretinib
Ripretinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
KIT/PDGFRA Switch-Control Inhibitor
≥98%
C24H21BrF2N4O2S
EUR-C108
Selpercatinib
Selpercatinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
RET Inhibitor
≥98%
C29H28FN7O3
EUR-C109
Avapritinib
Avapritinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
KIT/PDGFRA D842V Inhibitor
≥98%
C26H26FN9O
EUR-C110
Larotrectinib
Larotrectinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Pan-TRK (NTRK1/2/3) Inhibitor
≥98%
C21H22F2N6O2
EUR-C111
Dacomitinib
Dacomitinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
EGFRHER2
Pan-ERBB (EGFR/HER2/HER4) Covalent Inhibitor
≥98%
C24H25ClFN5O2
EUR-C112
Brigatinib
Brigatinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
EGFRALK
ALK/EGFR Inhibitor (2nd Gen)
≥98%
C29H39ClFN7O2P
EUR-C113
Alectinib
Alectinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
ALK
ALK Inhibitor (2nd Gen)
≥98%
C30H34N4O2
EUR-C114
Trametinib
Trametinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
MEK1/MEK2
MEK1/2 Inhibitor
≥98%
C26H23FIN5O4
EUR-C115
Crizotinib
Crizotinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
ALK
ALK/MET/ROS1 Inhibitor (1st Gen)
≥98%
C21H22Cl2FN5O
EUR-C116
Vandetanib
Vandetanib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
EGFRVEGFR
VEGFR2/EGFR/RET Multi-Kinase Inhibitor
≥98%
C22H24BrFN4O2
EUR-C117
Tazemetostat
Tazemetostat is a research-grade compound offered by EuroAsia RND for laboratory research use only.
EZH2 Inhibitor
≥98%
C34H44N4O4
EUR-C118
Irinotecan
Irinotecan is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Topoisomerase I Inhibitor
≥98%
C33H38N4O6 (liposomal formulation)
EUR-C119
Abiraterone
Abiraterone is a research-grade compound offered by EuroAsia RND for laboratory research use only.
CYP17A1 Inhibitor (Androgen Biosynthesis Inhibitor)
≥98%
C26H33NO2
EUR-C120
Relugolix
Relugolix is a research-grade compound offered by EuroAsia RND for laboratory research use only.
GnRH Receptor Antagonist
≥98%
C29H27F2N7O5S
EUR-C121
Darolutamide
Darolutamide is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Androgen Receptor (AR) Antagonist
≥98%
C24H19F2N5O2
EUR-C122
Apalutamide
Apalutamide is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Androgen Receptor (AR) Inhibitor
≥98%
C21H15F4N5O2S
EUR-C123
Sonidegib
Sonidegib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Smoothened (SMO) Antagonist / Hedgehog Pathway Inhibitor
≥98%
C26H26F3N3O2
EUR-C124
Lurbinectedin
Lurbinectedin is a research-grade compound offered by EuroAsia RND for laboratory research use only.
RNA Pol II Inhibitor / Selective DNA Alkylating Agent
≥98%
C41H44N4O10S
EUR-C125
Mitomycin
Mitomycin is a research-grade compound offered by EuroAsia RND for laboratory research use only.
DNA Alkylating Agent
≥98%
C15H18N4O5
EUR-C126
Trabectedin
Trabectedin is a research-grade compound offered by EuroAsia RND for laboratory research use only.
DNA Minor Groove Binder / RNA Synthesis Inhibitor
≥98%
C39H43N3O11S2
EUR-C127
Iobenguane I 131
Iobenguane I 131 is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Targeted Radiotherapy (I-131 / Norepinephrine Transporter)
≥95% (radiochemical)
C8H10[131I]N2
EUR-C128
Lutetium Lu 177 dotatate
Lutetium Lu 177 dotatate is a research-grade compound offered by EuroAsia RND for laboratory research use only.
SSTR-Targeted Peptide Receptor Radionuclide Therapy (Lu-177)
≥95% (radiochemical)
C65H92LuN14O19 (complex)
EUR-C129
Radium-223 dichloride
Radium-223 dichloride is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Alpha-Particle Bone-Targeting Radiotherapy (Ra-223)
≥95% (radiochemical)
223RaCl2
EUR-C130
Trifluridine + Tipiracil
Trifluridine + Tipiracil is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Thymidylate Synthase Inhibitor + Thymidine Phosphorylase Inhibitor
≥98%
C10H11F3N2O5 + C9H10ClN3O2
EUR-C131
Giredestrant
Giredestrant is a research-grade compound offered by EuroAsia RND for laboratory research use only.
Selective Estrogen Receptor Degrader (SERD)
≥98%
C29H26F2N2O3
EUR-C132
Varlitinib
Varlitinib is a research-grade compound offered by EuroAsia RND for laboratory research use only.
EGFRHER2
Pan-HER (EGFR/HER2) Reversible TKI
≥98%
C26H25ClN6O3
EUR-C133
ARV-471
ARV-471 is a research-grade compound offered by EuroAsia RND for laboratory research use only.
ERalpha PROTAC Degrader
≥98%
C43H51F2N7O7
EUR-C134
Pemrametostat
Pemrametostat is a research-grade compound offered by EuroAsia RND for laboratory research use only.
PRMT5 Inhibitor
≥98%
C27H35N5O4
EUR-C135
Veliparib
Weak PARP trapper; sensitises chemotherapy and radiotherapy. Ideal chemo/radio sensitizer — low trapping avoids added myelosuppressionMechanism of Action: PARP1/2 InhibitorPurity: ≥99% |
PARP1/PARP2
PARP1/2 Inhibitor
≥99%
C13H14N4O2
EUR-C136
Pamiparib
Potent PARP trapper with CNS penetration; active in brain tumours. CNS-penetrant — only clinical PARPi with proven brain exposureMechanism of Action: PARP1/2 InhibitorPurity: ≥99% |
PARP1/PARP2
PARP1/2 Inhibitor
≥99%
C16H17FN4O2
EUR-C137
Fuzuloparib
PARP trapper; approved in China for BRCA-mutated recurrent ovarian cancer 2021. First China-approved PARPi; maintenance indicationMechanism of Action: PARP1/2 InhibitorPurity: ≥99% |
PARP1/PARP2
PARP1/2 Inhibitor
≥99%
C20H19FN4O3
EUR-C138
Senaparib
PARP trapper; China Phase III maintenance ovarian. BRCA-independent activity in HRD+ tumorsMechanism of Action: PARP1/2 InhibitorPurity: ≥99% |
PARP1/PARP2
PARP1/2 Inhibitor
≥99%
C19H19FN4O3
EUR-C139
Simmiparib
PARP trapper; Phase II China for HRD+ solid tumors. Novel tricyclic scaffold with improved selectivityMechanism of Action: PARP1/2 InhibitorPurity: ≥99% |
PARP1/PARP2
PARP1/2 Inhibitor
≥99%
C21H22FN5O3
EUR-C140
Iniparib
First clinical PARPi but found non-selective in mechanism studies; key historical learning. Pivotal negative trial shaped PARPi selectivity requirementsMechanism of Action: PARP Inhibitor (weak/non-selective)
PARP1/PARP2
PARP Inhibitor (weak/non-selective)
≥99%
C7H5IN2O2
EUR-C141
Divarasib
Highly potent covalent G12C inhibitor; partnered with SHP2i for combination. Highest published potency among G12C inhibitorsMechanism of Action: KRAS G12C Covalent InhibitorPurity: ≥99% |
KRAS
KRAS G12C Covalent Inhibitor
≥99%
C32H36F2N6O3
EUR-C142
Glecirasib
Approved in China 2024; active in CNS mets. First China-approved KRAS G12C inhibitorMechanism of Action: KRAS G12C Covalent InhibitorPurity: ≥99% |
KRAS
KRAS G12C Covalent Inhibitor
≥99%
C29H31F3N6O3
EUR-C143
Opnurasib
Combined with JAB-3312 SHP2 inhibitor in Phase I/II China. SHP2i combination deepens responseMechanism of Action: KRAS G12C Covalent InhibitorPurity: ≥99% |
KRAS
KRAS G12C Covalent Inhibitor
≥99%
EUR-C144
Avutometinib
Allosteric RAF/MEK clamp — prevents feedback MAPK reactivation. Only RAF/MEK clamp — prevents paradoxical ERK reactivationMechanism of Action: RAF/MEK Clamp InhibitorPurity: ≥99% |
MEK1/MEK2
RAF/MEK Clamp Inhibitor
≥99%
C21H18BrFN4O3
EUR-C145
KRAS G12V inhibitor (RM-007)
Covalent G12V inhibitor; second-most-common KRAS mutation after G12D in pancreatic. KRAS G12V — major unmet needMechanism of Action: KRAS G12V Covalent InhibitorPurity: ≥99% |
KRAS
KRAS G12V Covalent Inhibitor
≥99%
EUR-C175
Eftilagimod alpha
LAG-3-Ig fusion protein that stimulates APC-mediated CD8+ T-cell activation. Soluble LAG-3 that stimulates rather than blocks — opposite MOA to antibodiesMechanism of Action: LAG-3 Agonist (immune stimulator)
LAG-3 Agonist (immune stimulator)
≥99%
Recombinant LAG-3-Ig
EUR-C185
Gefitinib
First EGFR TKI approved; reversible; exon 19 del / L858R. First EGFR TKI — established targeted therapy era in lung cancerMechanism of Action: 1st-Gen EGFR TKIPurity: ≥99% |
EGFR
1st-Gen EGFR TKI
≥99%
C22H24ClFN4O3
EUR-C186
Erlotinib
Reversible EGFR TKI; also approved pancreatic cancer + gemcitabine. Only EGFR inhibitor approved in pancreatic cancerMechanism of Action: 1st-Gen EGFR TKIPurity: ≥99% |
EGFR
1st-Gen EGFR TKI
≥99%
C22H23N3O4
EUR-C187
Lapatinib
Dual EGFR/HER2 reversible TKI; oral; combined with capecitabine and letrozole. First approved dual EGFR/HER2 oral TKIMechanism of Action: Reversible EGFR/HER2 Dual TKIPurity: ≥99% |
EGFRHER2
Reversible EGFR/HER2 Dual TKI
≥99%
C29H26ClFN4O4S
EUR-C188
Furmonertinib
3rd-gen irreversible EGFR TKI; China approved 2021; 1st-line NSCLC. China-approved 3rd-gen; Phase III vs osimertinibMechanism of Action: 3rd-Gen EGFR TKIPurity: ≥99% |
EGFR
3rd-Gen EGFR TKI
≥99%
C27H31FN6O2
EUR-C189
Aumolertinib
3rd-gen irreversible EGFR TKI; China approved 2021; CNS activity. Superior CNS penetration vs osimertinib in head-to-head dataMechanism of Action: 3rd-Gen EGFR TKIPurity: ≥99% |
EGFR
3rd-Gen EGFR TKI
≥99%
C27H28FN5O2S
EUR-C190
Lazertinib
3rd-gen CNS-penetrant EGFR TKI; combined with amivantamab (MARIPOSA trial). Lazertinib + amivantamab = first EGFR TKI + bispecific comboMechanism of Action: 3rd-Gen EGFR TKIPurity: ≥99% |
EGFR
3rd-Gen EGFR TKI
≥99%
C29H32FN7O2
EUR-C191
Sunvozertinib
Selective EGFR exon 20 insertion inhibitor; China approved 2024. China-approved exon 20 inhibitorMechanism of Action: EGFR Exon 20 Insertion TKIPurity: ≥99% |
EGFR
EGFR Exon 20 Insertion TKI
≥99%
C26H29FN6O3
EUR-C192
Zipalertinib
Selective oral EGFR exon 20 inhibitor; FDA BLA submitted 2024. FDA submission 2024 — next exon 20 approval candidateMechanism of Action: EGFR Exon 20 Insertion TKIPurity: ≥99% |
EGFR
EGFR Exon 20 Insertion TKI
≥99%
C28H32FN5O4
EUR-C202
Pyrotinib
Irreversible pan-HER TKI; China approved 2018 for HER2+ breast cancer. China-approved pan-HER TKI — strong HER2+ breast dataMechanism of Action: Pan-ERBB Covalent TKI (China)
Pan-ERBB Covalent TKI (China)
≥99%
C29H27FN4O4
EUR-C203
Poziotinib
Dual EGFR/HER2 exon 20 insertion inhibitor. Dual exon 20 coverage — uniqueMechanism of Action: EGFR/HER2 Exon 20 InhibitorPurity: ≥99% |
EGFRHER2
EGFR/HER2 Exon 20 Inhibitor
≥99%
C27H24Cl2FN5O3
EUR-C206
Lifirafenib
Pan-RAF inhibitor with EGFR inhibition; active in RAS-mutant cancers; combined with MEK inhibitor. Pan-RAF coverage including CRAF — RAS-mutant activityMechanism of Action: Pan-RAF + EGFR InhibitorPurity: ≥99% |
EGFR
Pan-RAF + EGFR Inhibitor
≥99%
C25H27F3N4O4S
EUR-C207
Naporafenib
Potent pan-RAF inhibitor; active in BRAF-mutant and NRAS-mutant melanoma; combined with MEK inhibitors. NRAS-mutant melanoma — high unmet needMechanism of Action: Pan-RAF InhibitorPurity: ≥99% |
Pan-RAF Inhibitor
≥99%
C23H22ClFN6O2S
EUR-C208
Belvarafenib
Pan-RAF; combined with cobimetinib for NRAS-mutant and NF1-mutant cancers. NRAS-mutant — combined with MEK inhibitorMechanism of Action: Pan-RAF InhibitorPurity: ≥99% |
Pan-RAF Inhibitor
≥99%
C23H20F3N5O3S
EUR-C209
Tovorafenib
Type II pan-RAF inhibitor; once-weekly dosing; FDA approved pediatric LGG 2024. First targeted therapy approved for pediatric low-grade glioma — once-weeklyMechanism of Action: Pan-RAF Inhibitor (once-weekly)
Pan-RAF Inhibitor (once-weekly)
≥99%
C23H21F3N4O4S
EUR-C210
Exarafenib
Next-gen pan-RAF; designed to overcome paradoxical activation; combined with binimetinib. Overcomes paradoxical MAPK activation — pan-RAF with MEK comboMechanism of Action: Pan-RAF InhibitorPurity: ≥99% |
Pan-RAF Inhibitor
≥99%
EUR-C211
Agerafenib
Selective pan-RAF inhibitor for non-V600 BRAF class 2/3 alterations. BRAF class 2/3 fusions — rare but actionableMechanism of Action: Pan-RAF InhibitorPurity: ≥99% |
Pan-RAF Inhibitor
≥99%
EUR-C212
Zibotentan
Note: not a RAF inhibitor — endothelin pathway; listed here as differentiation example. Endothelin-A pathway distinction from BRAF classMechanism of Action: Endothelin A Antagonist (not RAF)
Endothelin A Antagonist (not RAF)
≥99%
C24H28FN5O7S
EUR-C213
Pimasertib
Allosteric MEK1/2 inhibitor; combined with SAR245409 (PI3K). MEK + PI3K vertical combinationMechanism of Action: MEK1/2 InhibitorPurity: ≥99% |
MEK1/MEK2
MEK1/2 Inhibitor
≥99%
C17H20FN5O3S
EUR-C214
Refametinib
Oral MEK inhibitor; combined with sorafenib for HCC. HCC — MEK + VEGFR combinationMechanism of Action: MEK1/2 InhibitorPurity: ≥99% |
MEK1/MEK2
MEK1/2 Inhibitor
≥99%
C19H20BrF2N3O3
EUR-C215
Ulixertinib
First ERK1/2 inhibitor in clinical trials; overcomes MEK inhibitor resistance. First clinical ERK inhibitor — positioned for MEKi resistanceMechanism of Action: ERK1/2 InhibitorPurity: ≥99% |
ERK1/2 Inhibitor
≥99%
C25H24ClN3O3
EUR-C216
Ravoxertinib
ATP-competitive ERK1/2 inhibitor; Genentech compound; combined with cobimetinib. ERK + MEK dual inhibition overcomes adaptive resistanceMechanism of Action: ERK1/2 InhibitorPurity: ≥99% |
ERK1/2 Inhibitor
≥99%
C25H24ClN3O3
EUR-C217
Copanlisib
Intravenous pan-PI3K inhibitor; approved for relapsed follicular lymphoma. Only IV pan-PI3K inhibitor; avoids GI toxicityMechanism of Action: Pan-PI3K Inhibitor (IV)
PI3K
Pan-PI3K Inhibitor (IV)
≥99%
C23H27FN8O5
EUR-C218
Duvelisib
Oral dual PI3Kδ/γ inhibitor; approved CLL/SLL and follicular lymphoma. Dual δ/γ — targets both B-cell and T-cell/macrophage signalingMechanism of Action: PI3Kδ/γ Dual InhibitorPurity: ≥99% |
PI3K
PI3Kδ/γ Dual Inhibitor
≥99%
C24H25FN6O2S
EUR-C219
Idelalisib
First PI3Kδ inhibitor approved; B-cell malignancy focused. First PI3Kδ inhibitor — established PI3K class in oncologyMechanism of Action: PI3Kδ-Selective InhibitorPurity: ≥99% |
PI3K
PI3Kδ-Selective Inhibitor
≥99%
C22H18FN7O
EUR-C220
Umbralisib
PI3Kδ + CK1ε dual inhibitor; differentiated toxicity profile vs idelalisib. PI3Kδ + CK1ε — unique dual targetMechanism of Action: PI3Kδ + CK1ε Dual InhibitorPurity: ≥99% |
PI3K
PI3Kδ + CK1ε Dual Inhibitor
≥99%
C26H23FN6O3S
EUR-C221
Parsaclisib
Highly potent PI3Kδ inhibitor; intermittent dosing to manage toxicity. 10-fold more potent than idelalisibMechanism of Action: PI3Kδ-Selective Inhibitor (high potency)
PI3K
PI3Kδ-Selective Inhibitor (high potency)
≥99%
C22H22FN7O2
EUR-C222
Zandelisib
Intermittent dosing PI3Kδ inhibitor reduces immune-mediated toxicity. Intermittent dosing strategy reduces colitis and hepatitisMechanism of Action: PI3Kδ-Selective Inhibitor (intermittent)
PI3K
PI3Kδ-Selective Inhibitor (intermittent)
≥99%
C21H20FN5O3S
EUR-C223
Taselisib
β-sparing PI3K inhibitor; enriched activity in PIK3CA-mutant tumors. Beta-sparing design for PIK3CA-mutant enrichmentMechanism of Action: PI3Kα/β/δ Inhibitor (β-sparing)
PI3K
PI3Kα/β/δ Inhibitor (β-sparing)
≥99%
C23H24FN7O3S
EUR-C224
Serabelisib
PI3Kα-selective inhibitor; combined with fulvestrant for ER+ breast cancer. PI3Kα-selective — breast cancer backboneMechanism of Action: PI3Kα-Selective InhibitorPurity: ≥99% |
PI3K
PI3Kα-Selective Inhibitor
≥99%
C21H23F2N5O2S
EUR-C225
Miransertib
Pan-AKT inhibitor; specific Phase II data in Proteus syndrome (overgrowth) and PIK3CA/AKT-mutant cancers. Rare PIK3CA-AKT overgrowth disorders + cancerMechanism of Action: AKT1/2/3 InhibitorPurity: ≥99% |
AKT
AKT1/2/3 Inhibitor
≥99%
C20H21FN4O2
EUR-C226
Afuresertib
AKT inhibitor; combined with carfilzomib in multiple myeloma. AKT + proteasome inhibitor combinationMechanism of Action: Pan-AKT InhibitorPurity: ≥99% |
AKT
Pan-AKT Inhibitor
≥99%
C21H25ClN4O3S
EUR-C227
Uprosertib
AKT inhibitor; LOTUS/ZEAL trials in TNBC with MEK inhibitor. AKT + MEK combination in TNBCMechanism of Action: Pan-AKT InhibitorPurity: ≥99% |
AKT
Pan-AKT Inhibitor
≥99%
C20H22N4O3S
EUR-C228
Everolimus
Rapamycin analogue; allosteric mTORC1 inhibitor; approved in 6 cancer types. Broadest approved rapalogue; backbone with hormonal agentsMechanism of Action: mTORC1 Inhibitor (rapalogue)
mTOR
mTORC1 Inhibitor (rapalogue)
≥99%
C53H83NO14
EUR-C229
Temsirolimus
IV rapamycin ester; first mTOR inhibitor approved in oncology. First mTOR inhibitor approved in oncologyMechanism of Action: mTORC1 Inhibitor (rapalogue, IV)
mTOR
mTORC1 Inhibitor (rapalogue | IV)
≥99%
C56H87NO16
EUR-C230
Ridaforolimus
Non-prodrug rapamycin analogue; evaluated in sarcoma maintenance (SUCCEED trial). Non-prodrug rapalogue — established sarcoma mTOR biologyMechanism of Action: mTORC1 Inhibitor (non-prodrug rapalogue)
mTOR
mTORC1 Inhibitor (non-prodrug rapalogue)
≥99%
C53H81NO14
EUR-C231
Vistusertib
Selective dual mTORC1/2 inhibitor; overcomes mTORC2-AKT feedback. Dual mTORC1/2 — overcomes rapalogue feedback activationMechanism of Action: mTORC1/2 Dual InhibitorPurity: ≥99% |
mTOR
mTORC1/2 Dual Inhibitor
≥99%
C20H24FN5O3
EUR-C232
Dactolisib
Dual pan-PI3K and mTOR kinase inhibitor; simultaneous vertical pathway blockade. Simultaneous PI3K + mTOR — prevents mTOR-independent feedbackMechanism of Action: PI3K/mTOR Dual InhibitorPurity: ≥99% |
PI3KmTOR
PI3K/mTOR Dual Inhibitor
≥99%
C30H22N6O
EUR-C233
Apitolisib
Oral dual PI3K/mTOR; Genentech compound. Genentech PI3K/mTOR dual inhibitor — clinical benchmarkMechanism of Action: PI3K/mTOR Dual InhibitorPurity: ≥99% |
PI3KmTOR
PI3K/mTOR Dual Inhibitor
≥99%
C23H27N7O4
EUR-C234
Gedatolisib
IV dual PI3K/mTOR inhibitor; Pfizer compound; combined with palbociclib + letrozole. IV PI3K/mTOR + CDK4/6 triple combinationMechanism of Action: PI3K/mTOR Dual Inhibitor (IV)
PI3KmTOR
PI3K/mTOR Dual Inhibitor (IV)
≥99%
C31H36F2N8O4
EUR-C235
Omipalisib
Potent dual PI3K/mTOR inhibitor; also inhibits PI4Kβ. PI4Kβ inhibition unique among PI3K/mTOR dual agentsMechanism of Action: PI3K/mTOR Dual InhibitorPurity: ≥99% |
PI3KmTOR
PI3K/mTOR Dual Inhibitor
≥99%
C23H22FN5O3S
EUR-C236
Bimiralisib
CNS-penetrant dual PI3K/mTOR inhibitor; active in lymphoma and brain tumors. CNS-penetrant PI3K/mTOR — CNS lymphoma focusMechanism of Action: PI3K/mTOR Dual Inhibitor (CNS-penetrant)
PI3KmTOR
PI3K/mTOR Dual Inhibitor (CNS-penetrant)
≥99%
C18H22FN5O3
EUR-C237
Trilaciclib
First CDK4/6 inhibitor approved for myeloprotection (not anti-cancer per se); G1 arrest protects HSCs from chemo. Only CDK4/6i approved for myeloprotection — novel useMechanism of Action: CDK4/6 Inhibitor (myeloprotection)
CDK4/CDK6
CDK4/6 Inhibitor (myeloprotection)
≥99%
C25H33N9
EUR-C238
Lerociclib
CDK4/6 inhibitor; continuous dosing; Phase III data in ER+ breast vs palbociclib. Continuous vs intermittent dosing comparisonMechanism of Action: CDK4/6 Inhibitor (continuous dosing)
CDK4/CDK6
CDK4/6 Inhibitor (continuous dosing)
≥99%
C25H31FN8
EUR-C239
Dalpiciclib
China-approved CDK4/6 inhibitor for ER+HER2- breast cancer 2021. Third CDK4/6 inhibitor in ChinaMechanism of Action: CDK4/6 InhibitorPurity: ≥99% |
CDK4/CDK6
CDK4/6 Inhibitor
≥99%
C25H31FN8
EUR-C240
Samuraciclib
Non-covalent oral CDK7 inhibitor; combined with fulvestrant for ER+ breast. Non-covalent CDK7 — continuous dosing feasibleMechanism of Action: CDK7 Inhibitor (oral non-covalent)
CDK7 Inhibitor (oral non-covalent)
≥99%
C22H28FN5O2
EUR-C241
Atirmociclib
Pfizer selective CDK4 inhibitor (spares CDK6) — reduces neutropenia. CDK4-only selectivity reduces CDK6-mediated neutropenia — next-genMechanism of Action: CDK4-Selective InhibitorPurity: ≥99% |
CDK4/CDK6
CDK4-Selective Inhibitor
≥99%
EUR-C242
Zotiraciclib
CDK9-focused inhibitor; also inhibits CDK2 and CDK7; combined with paclitaxel for GBM. CDK9 focus for GBM — limited options in brain tumorsMechanism of Action: CDK9/2/7 InhibitorPurity: ≥99% |
CDK9/2/7 Inhibitor
≥99%
C22H25FN6O
EUR-C243
Voruciclib
Oral selective CDK9 inhibitor; combined with venetoclax for AML. CDK9 + BCL-2 combo — transcription + apoptosis blockadeMechanism of Action: CDK9 Inhibitor (oral)
CDK9 Inhibitor (oral)
≥99%
EUR-C244
Milciclib
Dual CDK2 and TRKA inhibitor; thymic carcinoma focus. Unique dual CDK2 + TRK coverage — thymic carcinoma focusMechanism of Action: CDK2/TRKA InhibitorPurity: ≥99% |
CDK2/TRKA Inhibitor
≥99%
C22H29N7O
EUR-C245
Seliciclib
First CDK2 inhibitor in clinical trials; nasal administration for NPC. First clinical CDK2 inhibitor — established CDK biologyMechanism of Action: CDK2/7/9 InhibitorPurity: ≥99% |
CDK2/7/9 Inhibitor
≥99%
C19H26N6O
EUR-C246
Abemaciclib
Unique CDK4/6i given continuously (not 3 weeks on/1 week off); approved for early breast cancer 2021. Only CDK4/6 inhibitor in early-stage breast cancer; continuous dosingMechanism of Action: CDK4/6 Inhibitor (unique: continuous dosing)
CDK4/CDK6
CDK4/6 Inhibitor (unique: continuous dosing)
≥99%
C27H32F2N8
EUR-C247
Zanubrutinib
Highly selective 2nd-gen BTK inhibitor; superior to ibrutinib in head-to-head ALPINE trial. First BTK inhibitor to beat ibrutinib head-to-head (ALPINE)
BTK
BTK Inhibitor (2nd-gen covalent)
≥99%
C27H29N5O2
EUR-C248
Orelabrutinib
China-approved selective BTK inhibitor; less off-target kinase inhibition. China 2nd-gen BTK inhibitor with improved selectivityMechanism of Action: BTK Inhibitor (2nd-gen covalent)
BTK
BTK Inhibitor (2nd-gen covalent)
≥99%
C28H29N5O2
EUR-C249
Tirabrutinib
BTK inhibitor; Japan approved for WM and CNS lymphoma — CNS penetrant. CNS-penetrant BTK — only approved for CNS lymphomaMechanism of Action: BTK Inhibitor (covalent, CNS-penetrant)
BTK
BTK Inhibitor (covalent | CNS-penetrant)
≥99%
C24H26FN7O2
EUR-C250
Vecabrutinib
Early non-covalent BTK inhibitor; active vs C481S resistance. Pioneered non-covalent BTK for C481S resistanceMechanism of Action: Non-Covalent BTK Inhibitor (1st-gen)
BTK
Non-Covalent BTK Inhibitor (1st-gen)
≥99%
EUR-C251
Fenebrutinib
Non-covalent reversible BTK inhibitor; autoimmune focus but oncology trials. Non-covalent BTK from GenentechMechanism of Action: Non-Covalent BTK InhibitorPurity: ≥99% |
BTK
Non-Covalent BTK Inhibitor
≥99%
C30H31FN6O2
EUR-C252
Nemtabrutinib
Non-covalent BTK inhibitor; also inhibits Src family kinases; active in ibrutinib-resistant CLL. BTK + Src family kinase — multi-target resistance preventionMechanism of Action: BTK Inhibitor + SRC/LynPurity: ≥99% |
BTK
BTK Inhibitor + SRC/Lyn
≥99%
C20H22FN7O3
EUR-C253
Tolebrutinib
CNS-penetrant reversible BTK inhibitor; primarily MS but oncology exploration. CNS-penetrant BTK — MS drug repurposed for CNS lymphomaMechanism of Action: Non-Covalent BTK Inhibitor (CNS)
BTK
Non-Covalent BTK Inhibitor (CNS)
≥99%
C25H22FN7O2S
EUR-C254
Elsubrutinib
AbbVie covalent BTK; combined with venetoclax for B-cell malignancies. BTK + BCL-2 combination approachMechanism of Action: BTK Inhibitor (covalent, selective)
BTK
BTK Inhibitor (covalent | selective)
≥99%
EUR-C255
Ensartinib
Potent 2nd-gen ALK inhibitor; active in brain mets; China/Europe approved. Strong CNS data in head-to-head vs crizotinib (eXalt3 trial)
ALK
ALK Inhibitor (2nd-gen)
≥99%
C23H24ClFN6O2
EUR-C256
Repotrectinib
Next-gen ROS1/TRK inhibitor; overcomes G2032R/CD74-ROS1 resistance; FDA approved 2023. Overcomes solvent-front resistance mutations — first approved for ROS1-resistant NSCLCMechanism of Action: ROS1/TRK/ALK Inhibitor (next-gen)
ALK
ROS1/TRK/ALK Inhibitor (next-gen)
≥99%
C22H24FN7O2
EUR-C257
Taletrectinib
Potent ROS1 + TRKA inhibitor; active vs ROS1 G2032R; China approved 2023. Second China-approved ROS1 inhibitor; non-macrocyclic scaffoldMechanism of Action: ROS1/TRKA Inhibitor (non-macrocyclic)
ROS1/TRKA Inhibitor (non-macrocyclic)
≥99%
C25H27FN6O3
EUR-C258
Selitrectinib
2nd-gen pan-TRK inhibitor; designed for kinase domain resistance mutations after larotrectinib. Overcomes TRK resistance mutations — resistance-mutation focused TRKiMechanism of Action: Pan-TRK Inhibitor (2nd-gen resistance)
Pan-TRK Inhibitor (2nd-gen resistance)
≥99%
EUR-C259
Cabozantinib
Multi-targeted kinase inhibitor; approved RCC (1st-line + combo), HCC, thyroid; anti-angiogenic + anti-MET. Most broadly approved multi-kinase TKIMechanism of Action: Multi-Kinase TKI (MET/VEGFR/RET/AXL)
EGFRVEGFR
Multi-Kinase TKI (MET/VEGFR/RET/AXL)
≥99%
C28H24FN3O5S
EUR-C260
Belizatinib
ALK + pan-TRK inhibitor; dual coverage for ALK and TRK fusions. Dual ALK + TRK coverageMechanism of Action: ALK/TRK InhibitorPurity: ≥99% |
ALK
ALK/TRK Inhibitor
≥99%
EUR-C261
Frizatinib
3rd-gen ALK inhibitor; overcomes lorlatinib-resistance ALK compound mutations. 4th ALK inhibitor generation — after lorlatinib resistanceMechanism of Action: ALK Inhibitor (3rd-gen)
ALK
ALK Inhibitor (3rd-gen)
≥99%
EUR-C262
Unecritinib
China 3rd-gen ALK/ROS1 inhibitor; active vs ALK compound mutations. China next-gen ALK inhibitorMechanism of Action: ALK Inhibitor (China 3rd-gen)
ALK
ALK Inhibitor (China 3rd-gen)
≥99%
EUR-C263
Merestinib
Multi-targeted type II kinase inhibitor; potent MET and RON inhibitor; combined with abemaciclib. RON receptor — rare addition to MET inhibitor classMechanism of Action: MET/RON/AXL/TIE2/TRKA InhibitorPurity: ≥99% |
MET/RON/AXL/TIE2/TRKA Inhibitor
≥99%
C26H27FN6O2
EUR-C264
Futibatinib
First covalent (irreversible) pan-FGFR inhibitor; overcomes FGFR resistance mutations. Only covalent FGFR inhibitor — overcomes FGFR resistance point mutationsMechanism of Action: FGFR1/2/3/4 Covalent InhibitorPurity: ≥99% |
FGFR1/2/3/4 Covalent Inhibitor
≥99%
C24H26F2N4O4S
EUR-C265
Tinengotinib
Novel compound combining FGFR inhibition with CDK4/6 and Aurora A. Triple FGFR + CDK + Aurora — overcomes multiple resistance nodesMechanism of Action: Pan-FGFR + CDK InhibitorPurity: ≥99% |
Pan-FGFR + CDK Inhibitor
≥99%
EUR-C266
Gunagratinib
Covalent pan-FGFR inhibitor; China development for FGFR-altered biliary. China covalent pan-FGFR inhibitorMechanism of Action: Pan-FGFR Covalent InhibitorPurity: ≥99% |
Pan-FGFR Covalent Inhibitor
≥99%
EUR-C267
Derazantinib
FGFR2-biased pan-FGFR inhibitor; EU approved biliary 2023. EU-approved FGFR2-biased — European data packageMechanism of Action: Pan-FGFR Inhibitor (FGFR2 bias)
Pan-FGFR Inhibitor (FGFR2 bias)
≥99%
EUR-C268
Fisogatinib
Highly selective FGFR4 inhibitor; for HCC with FGF19 amplification. Selective FGFR4 — HCC with FGF19-FGFR4 oncogenic axisMechanism of Action: FGFR4-Selective InhibitorPurity: ≥99% |
FGFR4-Selective Inhibitor
≥99%
EUR-C269
Savolitinib
Highly selective oral MET inhibitor; combined with osimertinib for MET-amplified NSCLC after EGFR TKI. MET + osimertinib combo for EGFR TKI resistance via MET amplificationMechanism of Action: MET-Selective InhibitorPurity: ≥99% |
MET-Selective Inhibitor
≥99%
C16H15FN6O
EUR-C270
Elzovantinib
Triple MET + SRC + CSF1R inhibitor; combines tumor cell + TME (macrophage) targeting. Simultaneous MET + immune TME targetingMechanism of Action: MET/SRC/CSF1R InhibitorPurity: ≥99% |
MET/SRC/CSF1R Inhibitor
≥99%
EUR-C271
Glesatinib
Multi-targeted MET/RON/VEGFR2 inhibitor. MET + RON + angiogenesisMechanism of Action: MET/RON/VEGFR2 InhibitorPurity: ≥99% |
EGFRVEGFR
MET/RON/VEGFR2 Inhibitor
≥99%
EUR-C275
Fruquintinib
Highly selective oral VEGFR1-3 TKI; minimal off-target; FDA approved mCRC 2023. Most selective VEGFR1-3 TKI approved — minimal off-target toxicityMechanism of Action: VEGFR1/2/3-Selective TKIPurity: ≥99% |
EGFRVEGFR
VEGFR1/2/3-Selective TKI
≥99%
C21H18ClFN4O4
EUR-C276
Anlotinib
Multi-target anti-angiogenic; China approved for NSCLC, SCLC, sarcoma, thyroid. China-approved multi-targeted anti-angiogenic — SCLC approvalMechanism of Action: Multi-Kinase VEGFR/FGFR/PDGFR/c-Kit TKIPurity: ≥99% |
EGFRVEGFR
Multi-Kinase VEGFR/FGFR/PDGFR/c-Kit TKI
≥99%
C21H23ClFN3O4
EUR-C277
Sunitinib
Multi-targeted TKI; approved GIST, PNET, RCC; broad anti-tumor spectrum. Early broad anti-angiogenic TKI — established multi-kinase classMechanism of Action: Multi-Kinase VEGFR/PDGFR/KIT/FLT3 TKIPurity: ≥99% |
EGFRVEGFR
Multi-Kinase VEGFR/PDGFR/KIT/FLT3 TKI
≥99%
C22H27FN4O2
EUR-C278
Sorafenib
First VEGFR + RAF inhibitor; approved HCC (1st approved systemic), RCC, thyroid. First approved systemic therapy for HCC — landmarkMechanism of Action: Multi-Kinase VEGFR/RAF/PDGFR TKIPurity: ≥99% |
EGFRVEGFR
Multi-Kinase VEGFR/RAF/PDGFR TKI
≥99%
C21H16ClF3N4O3
EUR-C279
Rivoceranib
Oral selective VEGFR2 inhibitor; combined with camrelizumab — FDA approved HCC 2023. First China VEGFR2 TKI with FDA approval in combinationMechanism of Action: VEGFR2-Selective TKI (oral)
EGFRVEGFR
VEGFR2-Selective TKI (oral)
≥99%
C22H21N3O4S
EUR-C280
Pazopanib
Multi-targeted TKI; approved RCC and soft-tissue sarcoma; comparable to sunitinib in RCC. COMPARZ trial: pazopanib = sunitinib in RCC efficacy — defined non-inferiorityMechanism of Action: Multi-Kinase VEGFR/PDGFR/KIT TKIPurity: ≥99% |
EGFRVEGFR
Multi-Kinase VEGFR/PDGFR/KIT TKI
≥99%
C21H23N7O2S
EUR-C281
Surufatinib
Multi-kinase inhibitor targeting angiogenesis + macrophage signaling; China approved NEN 2020. CSF1R addition adds macrophage TME targeting to anti-angiogenicMechanism of Action: VEGFR/FGFR1/CSF1R TKIPurity: ≥99% |
EGFRVEGFR
VEGFR/FGFR1/CSF1R TKI
≥99%
C23H22FN5O5S
EUR-C282
Linifanib
Anti-angiogenic multi-kinase inhibitor; AbbVie compound; compared to sorafenib in HCC. VEGFR + FLT3 — dual use in HCC and AMLMechanism of Action: VEGFR/PDGFR/KIT/FLT3 TKIPurity: ≥99% |
EGFRVEGFR
VEGFR/PDGFR/KIT/FLT3 TKI
≥99%
C22H17FN4O
EUR-C283
Ruxolitinib
First JAK inhibitor approved; myelofibrosis, PV, acute GvHD; topical for alopecia. First JAK inhibitor — established JAK-STAT in oncologyMechanism of Action: JAK1/JAK2 InhibitorPurity: ≥99% |
JAK1/JAK2 Inhibitor
≥99%
C17H18N6
EUR-C284
Pacritinib
JAK2/FLT3/IRAK1 inhibitor; no JAK1 activity — minimal anemia; approved thrombocytopenic MF. First JAK inhibitor for MF with severe thrombocytopenia — unique safetyMechanism of Action: JAK2/FLT3/IRAK1 Inhibitor (non-JAK1)
JAK2/FLT3/IRAK1 Inhibitor (non-JAK1)
≥99%
C28H32N4O3
EUR-C285
Momelotinib
JAK1/2 + ACVR1 inhibitor; ACVR1 inhibition corrects anemia in MF; FDA approved 2023. ACVR1 inhibition corrects MF anemia — unique mechanism in JAK classMechanism of Action: JAK1/JAK2 + ACVR1 InhibitorPurity: ≥99% |
JAK1/JAK2 + ACVR1 Inhibitor
≥99%
C23H22FN5O3
EUR-C286
Itacitinib
Selective JAK1 inhibitor; combined with ruxolitinib for treatment-naïve MF; GvHD focus. JAK1-selective — reduced metabolic side effectsMechanism of Action: JAK1-Selective InhibitorPurity: ≥99% |
JAK1-Selective Inhibitor
≥99%
C15H16FN5O
EUR-C287
Baricitinib
JAK1/2 inhibitor; RA approval; alopecia areata approval; COVID-19 emergency; now oncology exploration. JAK1/2 — broadest non-oncology approvals providing safety dataMechanism of Action: JAK1/JAK2 InhibitorPurity: ≥99% |
JAK1/JAK2 Inhibitor
≥99%
C16H17N7O2S
EUR-C288
Upadacitinib
Most selective JAK1 inhibitor; RA, Crohn's, UC; oncology repurposing for cutaneous lymphoma. High JAK1 selectivity — minimum JAK2 thrombocytopeniaMechanism of Action: JAK1-Selective InhibitorPurity: ≥99% |
JAK1-Selective Inhibitor
≥99%
C17H19F3N6O
EUR-C289
Filgotinib
Highly selective JAK1 inhibitor; RA and IBD approval; oncology exploration. JAK1 selectivity — IBD/RA drug repurposed in oncologyMechanism of Action: JAK1-Selective InhibitorPurity: ≥99% |
JAK1-Selective Inhibitor
≥99%
C16H17FN6O2
EUR-C290
Cerdulatinib
Dual JAK + SYK inhibitor; blocks BCR and JAK-STAT simultaneously in B-cell lymphoma. Dual JAK + SYK — simultaneous BCR and cytokine signaling blockadeMechanism of Action: JAK1/2/3 + SYK InhibitorPurity: ≥99% |
JAK1/2/3 + SYK Inhibitor
≥99%
C22H24FN7O2S
EUR-C291
Midostaurin
Multi-kinase inhibitor; first FLT3 inhibitor approved; combined with 7+3 chemo for FLT3-mut AML. First FLT3 inhibitor approval — combined with induction chemoMechanism of Action: FLT3/PKC Multi-Kinase InhibitorPurity: ≥99% |
FLT3/PKC Multi-Kinase Inhibitor
≥99%
C35H30N4O4
EUR-C292
Crenolanib
Type I FLT3 inhibitor; active vs TKD resistance mutations D835Y and F691L. Overcomes FLT3 TKD resistance after quizartinib/midostaurinMechanism of Action: FLT3 Inhibitor (ITD+TKD, type I)
FLT3 Inhibitor (ITD+TKD | type I)
≥99%
C26H30FN5O2
EUR-C293
Olutasidenib
Selective IDH1 R132 mutant inhibitor; FDA approved 2022 for R/R AML. Second IDH1 inhibitor approved — differentiation-inducingMechanism of Action: IDH1 Mutant Inhibitor (R132)
IDH1 Mutant Inhibitor (R132)
≥99%
C17H16F3N5O
EUR-C294
Enasidenib
IDH2 mutant inhibitor; FDA approved 2017 for R/R AML; differentiation therapy. First IDH2 inhibitor; established 2-HG oncometabolite targetingMechanism of Action: IDH2 Mutant InhibitorPurity: ≥99% |
IDH2 Mutant Inhibitor
≥99%
C19H17F3N8O
EUR-C295
Vorasidenib
CNS-penetrant dual IDH1/2 inhibitor; FDA approved 2024 for grade 2 IDH-mutant glioma. First targeted therapy approved for grade 2 glioma — IDH pan-inhibitorMechanism of Action: IDH1/2 Pan-Mutant Inhibitor (CNS-penetrant)
IDH1/2 Pan-Mutant Inhibitor (CNS-penetrant)
≥99%
C22H18F4N6
EUR-C296
Ziftomenib
Menin inhibitor; Phase II data in KMT2A-rearranged AND NPM1-mutated AML; impressive ORR. NPM1-mutated AML — expanded beyond KMT2A rearrangementMechanism of Action: Menin-KMT2A Interaction InhibitorPurity: ≥99% |
Menin-KMT2A Interaction Inhibitor
≥99%
EUR-C297
Bleximenib
J&J menin inhibitor; Phase I data in KMT2A-r AML/ALL with high ORR. All subtypes — AML + ALL coverageMechanism of Action: Menin-KMT2A Interaction InhibitorPurity: ≥99% |
Menin-KMT2A Interaction Inhibitor
≥99%
EUR-C298
Linperlisib
China PI3Kδ inhibitor; NMPA approved for relapsed/refractory FL 2023. China PI3Kδ — follicular lymphomaMechanism of Action: PI3Kδ Inhibitor (heme malignancies)
PI3K
PI3Kδ Inhibitor (heme malignancies)
≥99%
EUR-C299
Venetoclax
First BCL-2-selective inhibitor approved; combined with azacitidine for unfit AML; CLL backbone. Landmark BCL-2 inhibitor — redefined AML and CLL treatmentMechanism of Action: BCL-2 Selective InhibitorPurity: ≥99% |
BCL-2
BCL-2 Selective Inhibitor
≥99%
C45H50ClN7O7S
EUR-C300
Navitoclax
Pan-BCL-2 family inhibitor; thrombocytopenia from BCL-XL; combined with ruxolitinib for MF. BCL-2 + BCL-XL — thrombocytopenia limits monotherapy but drives combosMechanism of Action: BCL-2/BCL-XL/BCL-W InhibitorPurity: ≥99% |
BCL-2
BCL-2/BCL-XL/BCL-W Inhibitor
≥99%
C47H55ClN6O6S
EUR-C301
Pelabresib
BET inhibitor; combined with ruxolitinib for MF (MANIFEST Phase III 2024). BRD4 + JAK combination — new MF combination standard candidateMechanism of Action: BET/BRD4 InhibitorPurity: ≥99% |
BET/BRD4 Inhibitor
≥99%
C20H13F2N3O3S
EUR-C302
Imatinib
First approved TKI; revolutionised CML treatment; GIST backbone; proof-of-concept for targeted therapy. First TKI approved — changed oncology foreverMechanism of Action: BCR-ABL/c-KIT/PDGFR TKI (1st-gen)
BCR-ABL/c-KIT/PDGFR TKI (1st-gen)
≥99%
C29H31N7O
EUR-C303
Nilotinib
2nd-gen BCR-ABL inhibitor; more potent and selective than imatinib; active vs most imatinib-resistant mutations. More potent 2nd-gen — fewer side effects vs imatinibMechanism of Action: BCR-ABL TKI (2nd-gen)
BCR-ABL TKI (2nd-gen)
≥99%
C28H22F3N7O
EUR-C304
Dasatinib
Dual BCR-ABL + Src kinase inhibitor; CNS-penetrant; approved CML and Ph+ ALL in children. Dual BCR-ABL + Src — CNS penetrant for Ph+ ALLMechanism of Action: BCR-ABL/SRC/LYN TKI (2nd-gen)
BCR-ABL/SRC/LYN TKI (2nd-gen)
≥99%
C22H26ClN7O2S
EUR-C305
Bosutinib
BCR-ABL + Src inhibitor; approved 1st-line CML and after imatinib failure. Bosutinib has unique GIST vs imatinib profile — GI side effects instead of QTcMechanism of Action: BCR-ABL/SRC TKI (2nd-gen)
BCR-ABL/SRC TKI (2nd-gen)
≥99%
C26H29Cl2N5O3
EUR-C306
Asciminib
Allosteric BCR-ABL inhibitor binding myristoyl pocket (STAMP inhibitor); T315I active; FDA approved 2021. First STAMP inhibitor — allosteric BCR-ABL targeting; T315I active without ponatinib riskMechanism of Action: BCR-ABL STAMP Inhibitor (myristoyl pocket)
BCR-ABL STAMP Inhibitor (myristoyl pocket)
≥99%
C20H18ClF2N5O2
EUR-C307
Olverembatinib
3rd-gen BCR-ABL inhibitor; China approved for T315I CML 2021; active where ponatinib fails. China 3rd-gen T315I inhibitorMechanism of Action: BCR-ABL T315I TKI (3rd-gen China)
BCR-ABL T315I TKI (3rd-gen China)
≥99%
C28H27F3N6OS
EUR-C308
Imetelstat
Telomerase inhibitor; FDA approved 2024 for MDS (low-risk, transfusion-dependent). First telomerase inhibitor approved — new MDS mechanismMechanism of Action: Telomerase InhibitorPurity: ≥99% |
Telomerase Inhibitor
≥99%
Oligonucleotide
EUR-C309
Vorinostat
First HDAC inhibitor approved; histone deacetylase pan-inhibitor. First HDAC inhibitor — established epigenetic targetingMechanism of Action: Pan-HDAC InhibitorPurity: ≥99% |
Pan-HDAC Inhibitor
≥99%
C14H20N2O3
EUR-C310
Romidepsin
Cyclic depsipeptide natural product; Class I HDAC inhibitor; IV; approved CTCL and PTCL. Natural product HDAC inhibitor — distinct scaffoldMechanism of Action: Class I HDAC Inhibitor (cyclic depsipeptide)
Class I HDAC Inhibitor (cyclic depsipeptide)
≥99%
C36H52N4O8S2
EUR-C311
Belinostat
Pan-HDAC inhibitor; approved PTCL 2014; combined with CHOP. T-cell lymphoma HDAC inhibitorMechanism of Action: Pan-HDAC InhibitorPurity: ≥99% |
Pan-HDAC Inhibitor
≥99%
C15H13N3O4S
EUR-C312
Panobinostat
Most potent pan-HDAC inhibitor; combined with bortezomib + dexamethasone for MM. Most potent pan-HDAC; myeloma indicationMechanism of Action: Pan-HDAC Inhibitor (most potent)
Pan-HDAC Inhibitor (most potent)
≥99%
C21H23N3O2
EUR-C313
Mocetinostat
Selective Class I/IV HDAC inhibitor; combined with gemcitabine for AML. Class I selective — reduced cardiac toxicity vs pan-HDACMechanism of Action: Class I + IV HDAC InhibitorPurity: ≥99% |
Class I + IV HDAC Inhibitor
≥99%
C24H22N6O
EUR-C314
Tucidinostat
China-approved HDAC inhibitor; PTCL; combined with exemestane for ER+ breast. Combined with aromatase inhibitor — ER+ breast cancer epigenetic comboMechanism of Action: Class I HDAC Inhibitor (China)
Class I HDAC Inhibitor (China)
≥99%
C22H19FN4O2
EUR-C315
Valproic acid
Weak non-selective HDAC inhibitor; antiepileptic repurposed; AML differentiation. Repurposed antiepileptic — AML differentiation proof of conceptMechanism of Action: HDAC Inhibitor (weak, non-selective)
HDAC Inhibitor (weak | non-selective)
≥99%
C8H16O2
EUR-C316
Valemetostat
Dual EZH1/2 inhibitor; Japan approved for R/R ATLL 2021 and PTCL 2023. Dual EZH1/2 inhibition — prevents EZH1 compensationMechanism of Action: EZH1/2 Dual InhibitorPurity: ≥99% |
EZH1/2 Dual Inhibitor
≥99%
C28H37FN6O2S
EUR-C317
Azacitidine
DNA hypomethylating agent; MDS, AML backbone; combined with venetoclax. First hypomethylating agent approved — MDS standard of careMechanism of Action: DNMT InhibitorPurity: ≥99% |
DNMT Inhibitor
≥99%
C8H12N4O5
EUR-C318
Guadecitabine
Dinucleotide DNMT inhibitor; resistant to cytidine deaminase — prolonged DNA exposure. Protects from CDA degradation — longer epigenetic exposureMechanism of Action: Next-gen DNMT Inhibitor (dinucleotide)
Next-gen DNMT Inhibitor (dinucleotide)
≥99%
C18H26N6O9
EUR-C319
Pinometostat
First selective DOT1L inhibitor in clinical trials; MLL-rearranged leukemia — H3K79 methylation. First DOT1L inhibitor — H3K79 methylation in MLL-fusion leukemiaMechanism of Action: DOT1L InhibitorPurity: ≥99% |
DOT1L Inhibitor
≥99%
C29H41N7O3S
EUR-C320
Pelabresib
BRD4 inhibitor; Phase III MANIFEST-2 in MF combined with ruxolitinib. Positive Phase III data with ruxolitinib — MF combinationMechanism of Action: BET/BRD4 InhibitorPurity: ≥99% |
BET/BRD4 Inhibitor
≥99%
C20H13F2N3O3S
EUR-C321
Molibresib
Pan-BET bromodomain inhibitor; NUT carcinoma focus where BRD4-NUT fusion is oncogenic. BRD4-NUT fusion — rare but highly BET-dependentMechanism of Action: Pan-BET InhibitorPurity: ≥99% |
Pan-BET Inhibitor
≥99%
C21H23FN4O4S
EUR-C322
Iadademstat
Selective LSD1 inhibitor; combined with azacitidine for AML (promising Phase I data 2023). LSD1 — transcription factor complex; SCLC dependencyMechanism of Action: LSD1 (KDM1A) InhibitorPurity: ≥99% |
LSD1 (KDM1A) Inhibitor
≥99%
C16H18FN3
EUR-C323
Bomedemstat
Oral LSD1 inhibitor; Phase II for essential thrombocythemia and MF. ET and MF — myeloproliferative LSD1 inhibitionMechanism of Action: LSD1 (KDM1A) InhibitorPurity: ≥99% |
LSD1 (KDM1A) Inhibitor
≥99%
EUR-C324
Bortezomib
First proteasome inhibitor approved; covalent boronic acid; backbone of MM therapy. First proteasome inhibitor — redefined myeloma treatmentMechanism of Action: 26S Proteasome Inhibitor (covalent)
26S Proteasome Inhibitor (covalent)
≥99%
C19H25BN4O4
EUR-C325
Carfilzomib
Second-generation irreversible proteasome inhibitor; no peripheral neuropathy; active after bortezomib resistance. Irreversible — no peripheral neuropathy; overcomes bortezomib resistanceMechanism of Action: 26S Proteasome Inhibitor (irreversible)
26S Proteasome Inhibitor (irreversible)
≥99%
C40H57N5O7
EUR-C326
Ixazomib
First oral proteasome inhibitor; combined with lenalidomide + dexamethasone. First oral proteasome inhibitor — home administrationMechanism of Action: 26S Proteasome Inhibitor (oral)
26S Proteasome Inhibitor (oral)
≥99%
C14H19BCl2N2O4
EUR-C327
Marizomib
Pan-proteasome inhibitor (all 3 sites); irreversible; CNS-penetrant for GBM. Pan-site proteasome + CNS penetration — uniqueMechanism of Action: 20S Proteasome Inhibitor (all 3 catalytic sites, CNS)
20S Proteasome Inhibitor (all 3 catalytic sites | CNS)
≥99%
C13H16ClNO4
EUR-C328
Pevonedistat
First NAE inhibitor; blocks neddylation pathway preventing Cullin-RING E3 ubiquitin ligase activation. Neddylation inhibition — upstream of proteasome; novelMechanism of Action: NEDD8-Activating Enzyme (NAE) InhibitorPurity: ≥99% |
NEDD8-Activating Enzyme (NAE) Inhibitor
≥99%
C21H25N5O3S
EUR-C329
Navitoclax
Pan-BCL-2 family; thrombocytopenia from BCL-XL on platelets limits monotherapy. BCL-XL — SCLC dependency; MF fibrosis regressionMechanism of Action: BCL-2/BCL-XL/BCL-W InhibitorPurity: ≥99% |
BCL-2
BCL-2/BCL-XL/BCL-W Inhibitor
≥99%
C47H55ClN6O6S
EUR-C330
Sonrotoclax
Next-gen BCL-2 inhibitor; more potent than venetoclax; combined with zanubrutinib for CLL. More potent BCL-2 inhibitor than venetoclax — next generationMechanism of Action: BCL-2 Inhibitor (next-gen, more potent)
BCL-2
BCL-2 Inhibitor (next-gen | more potent)
≥99%
EUR-C331
Idasanutlin
Potent MDM2 inhibitor; combined with venetoclax for AML; restores p53 tumor suppressor function. MDM2 + BCL-2 combination — p53 reactivation + apoptosisMechanism of Action: MDM2-p53 Interaction InhibitorPurity: ≥99% |
MDM2-p53 Interaction Inhibitor
≥99%
C27H23ClF4N2O5
EUR-C332
Navtemadlin
Potent oral MDM2 inhibitor; combined with venetoclax or MEK inhibitors. Novel scaffold MDM2 inhibitor — uveal melanoma focusMechanism of Action: MDM2 Inhibitor (piperidinyl oxindole)
MDM2 Inhibitor (piperidinyl oxindole)
≥99%
EUR-C333
Siremadlin
Novartis MDM2 inhibitor; combined with ribociclib (CDK4/6i) for TP53-WT solid tumors. MDM2-amplified liposarcoma — MDM2 amplification is oncogenic not just p53 lossMechanism of Action: MDM2 InhibitorPurity: ≥99% |
MDM2 Inhibitor
≥99%
EUR-C334
Milademetan
Potent MDM2 inhibitor; Phase II data in liposarcoma with MDM2 amplification. Liposarcoma — MDM2 amplification present in ~90% dedifferentiated LSMechanism of Action: MDM2 InhibitorPurity: ≥99% |
MDM2 Inhibitor
≥99%
EUR-C335
Glasdegib
Oral SMO inhibitor; approved with LDAC for unfit AML — first Hedgehog inhibitor in AML. Hedgehog inhibitor approved in AML — different from BCC indication of vismodegibMechanism of Action: Hedgehog/SMO Inhibitor (AML)
Hedgehog/SMO Inhibitor (AML)
≥99%
C21H22N6
EUR-C336
Taladegib
2nd-gen SMO inhibitor; active in vismodegib-resistant tumors with SMO D473H. Overcomes vismodegib resistance SMO mutationsMechanism of Action: SMO Inhibitor (2nd-gen)
SMO Inhibitor (2nd-gen)
≥99%
C24H21F3N4O
EUR-C337
Itraconazole
Antifungal with off-target SMO and VEGFR2 inhibition; repurposed cancer. Antifungal repurposed — SMO non-covalent inhibitionMechanism of Action: SMO Inhibitor (off-target)
SMO Inhibitor (off-target)
≥99%
C35H38Cl2N4O4
EUR-C339
Lutetium
PSMA-targeted peptide radioligand therapy; FDA approved 2022 for mCRPC. PSMA RLT — transformed mCRPC treatment; improved OS in TheraP/VISIONMechanism of Action: PSMA-Targeted Radiotherapy (Lu-177)
PSMA-Targeted Radiotherapy (Lu-177)
≥99%
C49H74LuN9O15
EUR-C340
Elacestrant
First oral SERD approved; active in ESR1-mutated ER+ breast cancer after CDK4/6 + AI. First oral SERD — overcomes ESR1 mutations causing AI resistanceMechanism of Action: SERD (Oral ER Degrader)
SERD (Oral ER Degrader)
≥99%
C30H33FN2O
EUR-C341
Camizestrant
AstraZeneca SERD; combined with CDK4/6 inhibitors in Phase III SERENA trials. Phase III data vs fulvestrant + CDK4/6 inhibitorMechanism of Action: SERD (Oral next-gen)
SERD (Oral next-gen)
≥99%
C30H34F2N2O
EUR-C342
Imlunestrant
Eli Lilly SERD; Phase III EMBER-3 data vs standard endocrine therapy. Lilly SERD — EMBER-3 Phase III ESR1-mutated patientsMechanism of Action: SERD (Oral, Lilly)
SERD (Oral | Lilly)
≥99%
EUR-C343
Lasofoxifene
Tissue-selective ER modulator; ELAINE trial for ESR1-mutated ER+ breast. SERM repositioned for ESR1-mutant breast — oral tissue-selective approachMechanism of Action: SERM (Selective ER Modulator)
SERM (Selective ER Modulator)
≥99%
C28H29NO2
EUR-C344
Fulvestrant
First ER degrader; IM injection; combined with CDK4/6 inhibitors; historical gold standard. First ER degrader — established SERD class; now replaced by oral SERDsMechanism of Action: ER Degrader (intramuscular SERD)
ER Degrader (intramuscular SERD)
≥99%
C32H47F5O3S
EUR-C345
Onapristone
PR antagonist; Phase II data in PR+ endometrial and breast cancers. PR-targeted therapy — progesterone receptor as oncology targetMechanism of Action: Progesterone Receptor AntagonistPurity: ≥99% |
Progesterone Receptor Antagonist
≥99%
EUR-C346
Orteronel
Non-steroidal CYP17A1 (17,20-lyase selective) inhibitor; less mineralocorticoid excess than abiraterone. 17,20-lyase selectivity — less hypertension/hypokalemia than abirateroneMechanism of Action: CYP17A1 Inhibitor (non-steroidal)
CYP17A1 Inhibitor (non-steroidal)
≥99%
C16H17N3O2
EUR-C347
Seviteronel
Lyase-selective CYP17A1 inhibitor; also directly inhibits AR. Dual CYP17A1 lyase + AR inhibitionMechanism of Action: CYP17A1 Lyase-Selective InhibitorPurity: ≥99% |
CYP17A1 Lyase-Selective Inhibitor
≥99%
EUR-C348
Proxalutamide
AR antagonist + degrader; markedly reduces AR protein levels; potent in CRPC. AR degradation beyond antagonism — next-gen AR targetingMechanism of Action: AR DegraderPurity: ≥99% |
AR Degrader
≥99%
EUR-C349
Bicalutamide
1st-gen AR antagonist; agonist switch in high AR — superseded by enzalutamide class. 1st-gen AR — agonist switch mechanism drove 2nd-gen developmentMechanism of Action: AR Antagonist (1st-gen)
AR Antagonist (1st-gen)
≥99%
C18H14F4N2O4S
EUR-C350
Elimusertib
Potent ATR inhibitor; combined with olaparib or avelumab; Bayer compound. ATR + PARPi combination — replication stress double-hitMechanism of Action: ATR Kinase InhibitorPurity: ≥99% |
ATR Kinase Inhibitor
≥99%
C22H24FN7O2
EUR-C351
Tuvusertib
Merck ATR inhibitor; combined with olaparib or avelumab. ATR + PARP combination — replication stressMechanism of Action: ATR InhibitorPurity: ≥99% |
ATR Inhibitor
≥99%
EUR-C352
Prexasertib
Potent CHK1/2 inhibitor; combined with PARP inhibitors and DNA damaging agents. CHK1/2 — replication checkpoint; PARPi combo synergyMechanism of Action: CHK1/CHK2 InhibitorPurity: ≥99% |
CHK1/CHK2 Inhibitor
≥99%
C26H28Cl2FN5O
EUR-C353
Rabusertib
Selective CHK1 inhibitor; combined with gemcitabine for solid tumors. Gemcitabine sensitisation via CHK1Mechanism of Action: CHK1 Inhibitor (selective)
CHK1 Inhibitor (selective)
≥99%
EUR-C354
Barasertib
Selective Aurora B inhibitor; IV prodrug; inhibits histone H3 phosphorylation. Aurora B-selective vs alisertib (Aurora A) — different mitotic mechanismMechanism of Action: Aurora B Kinase InhibitorPurity: ≥99% |
Aurora B Kinase Inhibitor
≥99%
C24H25FN8O3S
EUR-C355
Danusertib
Pan-Aurora + multi-kinase; combined with docetaxel. Pan-Aurora + ABL — unique dual cell cycle + oncogenic kinaseMechanism of Action: Pan-Aurora (A/B/C) + ABL/RET InhibitorPurity: ≥99% |
Pan-Aurora (A/B/C) + ABL/RET Inhibitor
≥99%
C27H28N6O2
EUR-C356
Rigosertib
Allosteric PLK1 + PI3K inhibitor; MDS Phase III; unusual non-ATP competitive MOA. Non-ATP competitive PLK1 — unique allosteric bindingMechanism of Action: PLK1/PI3K Inhibitor (non-ATP)
PI3K
PLK1/PI3K Inhibitor (non-ATP)
≥99%
C21H25NO5S2
EUR-C357
Ispinesib
Kinesin spindle protein (Eg5/KIF11) inhibitor; blocks mitotic spindle formation; taxane-independent. Taxane-independent mitotic arrest via Eg5Mechanism of Action: KSP/Eg5 (Kinesin) InhibitorPurity: ≥99% |
KSP/Eg5 (Kinesin) Inhibitor
≥99%
C26H35N3O
EUR-C358
Ganetespib
Potent HSP90 inhibitor; combined with docetaxel in NSCLC (GALAXY-2). Most advanced HSP90 inhibitor in Phase IIIMechanism of Action: HSP90 Inhibitor (resorcinol)
HSP90 Inhibitor (resorcinol)
≥99%
C24H26N4O4
EUR-C359
Luminespib
Potent IV HSP90 inhibitor; active in ALK-rearranged and HER2-mutated NSCLC. HER2-mutated NSCLC — HSP90 stabilises HER2 kinase domainMechanism of Action: HSP90 Inhibitor (isoxazole)
HSP90 Inhibitor (isoxazole)
≥99%
C26H31IN4O4
EUR-C360
Onalespib
Long-acting HSP90 inhibitor; once-weekly dosing; combined with imatinib for GIST. Long PK allows weekly dosing — client protein degradation persistsMechanism of Action: HSP90 Inhibitor (long-acting)
HSP90 Inhibitor (long-acting)
≥99%
C22H24F2N4O3
EUR-C361
Retaspimycin
Water-soluble geldanamycin analogue; IV; GIST and lung cancer trials. Geldanamycin derivative — reduced hepatotoxicity vs 17-AAGMechanism of Action: HSP90 Inhibitor (17-AAG analogue)
HSP90 Inhibitor (17-AAG analogue)
≥99%
C31H43N2O7S
EUR-C362
Tanespimycin
First HSP90 inhibitor in clinical trials; geldanamycin derivative; combined with bortezomib in MM. First clinical HSP90 inhibitor — established proof of conceptMechanism of Action: HSP90 Inhibitor (benzoquinone ansamycin)
HSP90 Inhibitor (benzoquinone ansamycin)
≥99%
C31H43N2O8Cl
EUR-C390
Vepdegestrant
ER PROTAC via CRBN; combined with palbociclib Phase III EMBER-4. PROTAC ER degrader — deeper ER degradation than SERDsMechanism of Action: ER PROTAC DegraderPurity: ≥99% |
ER PROTAC Degrader
≥99%
C43H51F2N7O7
EUR-C391
Lenalidomide
Immunomodulatory drug (IMiD); recruits CRBN to degrade Ikaros/Aiolos; also CK1α (del5q MDS). Molecular glue mechanism elucidated post-approval — foundational CRBN biologyMechanism of Action: IKZF1/IKZF3 Molecular Glue (CRL4-CRBN)
IKZF1/IKZF3 Molecular Glue (CRL4-CRBN)
≥99%
C13H13N3O3
EUR-C392
Pomalidomide
3rd-gen IMiD; more potent than lenalidomide; combined with bortezomib + dexamethasone. 3rd-gen IMiD — MMR-active in lenalidomide-refractory MMMechanism of Action: IKZF1/IKZF3 Molecular Glue (CRL4-CRBN)
IKZF1/IKZF3 Molecular Glue (CRL4-CRBN)
≥99%
C13H11N3O4
EUR-C393
Thalidomide
First IMiD/CRBN molecular glue; MM and ENL; teratogenicity from SALL4 degradation. First approved molecular glue — SALL4 mechanism explains teratogenicityMechanism of Action: IKZF1/IKZF3/SALL4 Molecular GluePurity: ≥99% |
IKZF1/IKZF3/SALL4 Molecular Glue
≥99%
C13H10N2O4
EUR-C394
Epacadostat
IDO1 inhibitor; tryptophan pathway; combined with pembrolizumab — Phase III negative (ECHO-301). IDO1 failure informed tryptophan pathway complexity — key biomarker lessonMechanism of Action: IDO1 InhibitorPurity: ≥99% |
IDO1 Inhibitor
≥99%
C14H11BrFN3O5S2
EUR-C395
Navoximod
IDO1 inhibitor; combined with atezolizumab. IDO1 + PD-L1 combination despite ECHO-301 resultsMechanism of Action: IDO1 InhibitorPurity: ≥99% |
IDO1 Inhibitor
≥99%
C13H11FN2O2
EUR-C396
Linrodostat
BMS IDO1 inhibitor; combined with nivolumab + ipilimumab. BMS IDO1 — still evaluated in multiple combinationsMechanism of Action: IDO1 Inhibitor (BMS)
IDO1 Inhibitor (BMS)
≥99%
C20H17FN4O
EUR-C397
Telaglenastat
Glutaminase inhibitor combined with nivolumab; ENTRATA trial in RCC. Glutamine deprivation + checkpoint — metabolic + immune comboMechanism of Action: GLS1 + checkpoint combinationPurity: ≥99% |
GLS1 + checkpoint combination
≥99%
EUR-C398
Mitapivat
Pyruvate kinase R activator for thalassemia/SCD; being repurposed for tumor glycolysis modulation. PKR activation — energy metabolism modulationMechanism of Action: PKR (Pyruvate Kinase R) ActivatorPurity: ≥99% |
PKR (Pyruvate Kinase R) Activator
≥99%
C22H24FN3O3S
EUR-C399
Actinium
Alpha-particle PSMA-targeted therapy; more potent than Lu-177; active post-Lu-177 failure. Alpha particle PSMA therapy — 100x more potent than beta; post-Lu-177 rescueMechanism of Action: PSMA-Targeted Alpha TherapyPurity: ≥99% |
PSMA-Targeted Alpha Therapy
≥99%
Small molecule + radionuclide
EUR-C400
Lutetium
Lu-177 FAP inhibitor RLT; FAP overexpressed on cancer-associated fibroblasts — pan-tumor. FAP — cancer-associated fibroblasts; pan-tumor stromal targetMechanism of Action: FAP-Targeted RLTPurity: ≥99% |
FAP-Targeted RLT
≥99%
Small molecule + 177Lu
EUR-C403
Ziftomenib
Menin inhibitor showing activity in NPM1-mutated AML — expanded beyond KMT2A. NPM1-mutated AML — 35% of AML patients; new indication for menin inhibitorsMechanism of Action: Menin Inhibitor (NPM1-mutated AML)
Menin Inhibitor (NPM1-mutated AML)
≥99%
EUR-C408
Motixafortide
Cyclic CXCR4 antagonist; approved for HSCT stem cell mobilization 2023; oncology combinations. FDA-approved CXCR4 antagonist — stem cell mobilization and AML bone marrow egressMechanism of Action: CXCR4 Antagonist (peptide)
CXCR4 Antagonist (peptide)
≥99%
Cyclic peptide
EUR-C414
Selpercatinib
RET inhibitor used as neoadjuvant therapy before surgery for RET-fusion thyroid cancer. Neoadjuvant targeted therapy for thyroid — shrinks tumor before surgeryMechanism of Action: RET Inhibitor NeoadjuvantPurity: ≥99% |
RET Inhibitor Neoadjuvant
≥99%
EUR-C415
Lorlatinib
First-line lorlatinib approved for ALK+ NSCLC 2021 — superior to crizotinib. Lorlatinib 1st-line — prevents resistance that develops with 1st/2nd-gen ALK inhibitorsMechanism of Action: 3rd-Gen ALK TKI (1st-line)
ALK
3rd-Gen ALK TKI (1st-line)
≥99%
EUR-C416
Alectinib
First-line alectinib approved 2017 — replaced crizotinib as preferred 1st-line ALK. Alectinib 1st-line — superior CNS efficacy vs crizotinibMechanism of Action: 2nd-Gen ALK TKI (1st-line)
ALK
2nd-Gen ALK TKI (1st-line)
≥99%
EUR-C417
Brigatinib
1st-line brigatinib approved for ALK+ NSCLC 2020. Brigatinib 1st-line — ALTA-1L superior to crizotinibMechanism of Action: 2nd-Gen ALK + EGFR TKI (1st-line)
EGFRALK
2nd-Gen ALK + EGFR TKI (1st-line)
≥99%
