PDGFR inhibitors

Protein Tyrosine Kinase

Isoform-selective Products

• All (62)
• PDGFR Inhibitors (61)
• PDGFR Antagonist (1)
• New PDGFR Products

Cat.No.	Product Name	Information	Product Use Citations	Product Validations
S7397	Sorafenib (BAY 43-9006)	Sorafenib is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Mol Cancer, 2025, 24(1):34 Nat Commun, 2025, 16(1):509 Adv Sci (Weinh), 2025, 12(30):e04372
S2475	Imatinib	Imatinib is a multi-target inhibitor of tyrosine kinase with inhibition for v-Abl, c-Kit and PDGFR, IC50 values are 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively. Imatinib (STI571) induces autophagy.	Cancer Cell, 2025, 43(4):776-796.e14 Theranostics, 2025, 15(8):3589-3609 Genome Med, 2025, 17(1):14
S1040	Sorafenib tosylate	Sorafenib tosylate is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. This compound inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. It induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Int J Oncol, 2025, 67(3)72 Nature, 2024, 629(8013):927-936 Cell Mol Life Sci, 2024, 81(1):238
S1026	Imatinib (STI571) Mesylate	Imatinib Mesylate is an orally bioavailability mesylate salt of Imatinib, which is a multi-target inhibitor of v-Abl, c-Kit and PDGFR with IC50 of 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively. Imatinib Mesylate (STI571) induces autophagy.	Sci Immunol, 2025, 10(109):eads5818 Blood Adv, 2025, bloodadvances.2024015364 Eur J Med Chem, 2025, 284:117211
S7781	Sunitinib (SU-11248)	Sunitinib is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM, and also inhibits c-Kit. Sunitinib is also a dose-dependent inhibitor of the autophosphorylation activity of IRE1α. Sunitinib induces autophagy and apoptosis.	Cancer Cell, 2025, 43(4):776-796.e14 Mol Cancer, 2025, 24(1):179 J Exp Clin Cancer Res, 2025, 44(1):290
S1490	Ponatinib (AP24534)	Ponatinib is a novel, potent multi-target inhibitor of Abl, PDGFRα, VEGFR2, FGFR1 and Src with IC50 of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM and 5.4 nM in cell-free assays, respectively. Ponatinib (AP24534) inhibits autophagy.	Nat Commun, 2025, 16(1):471 Theranostics, 2025, 15(8):3589-3609 J Exp Clin Cancer Res, 2025, 44(1):290
S1178	Regorafenib (BAY 73-4506)	Regorafenib is a multi-target inhibitor for VEGFR1, VEGFR2, VEGFR3, PDGFRβ, Kit (c-Kit), RET (c-RET) and Raf-1 with IC50 of 13 nM/4.2 nM/46 nM, 22 nM, 7 nM, 1.5 nM and 2.5 nM in cell-free assays, respectively. Regorafenib induces autophagy.	Nat Commun, 2025, 16(1):509 Cell Death Differ, 2025, 10.1038/s41418-025-01536-1 Cell Mol Gastroenterol Hepatol, 2025, S2352-345X(25)00026-8
S1005	Axitinib (AG-013736)	Axitinib is a multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFRβ and c-Kit with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM in Porcine aorta endothelial cells, respectively.	Cancer Cell, 2025, S1535-6108(25)00070-4 Chem Biol Interact, 2025, 418:111628 Development, 2025, 152(13)dev204684
S1042	Sunitinib malate	Sunitinib malate is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM in cell-free assays, and also inhibits c-Kit. Sunitinib Malate effectively inhibits autophosphorylation of Ire1α. Sunitinib Malate increases both death receptor and mitochondrial-dependent apoptosis.	CNS Neurosci Ther, 2025, 31(12):e70696 Sci Rep, 2025, 15(1):35889 Cell Oncol (Dordr), 2024, 10.1007/s13402-024-00939-5
S1010	Nintedanib (BIBF 1120)	Nintedanib is a potent triple angiokinase inhibitor for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β with IC50 of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM in cell-free assays. Phase 3.	Nat Commun, 2025, 16(1):471 Cell Death Dis, 2025, 16(1):196 Eur J Pharmacol, 2025, 1005:178058
S1164	Lenvatinib (E7080)	Lenvatinib is a multi-target inhibitor, mostly for VEGFR2(KDR)/VEGFR3(Flt-4) with IC50 of 4 nM/5.2 nM, less potent against VEGFR1/Flt-1, ~10-fold more selective for VEGFR2/3 against FGFR1, PDGFRα/β in cell-free assays. This compound also inhibits FGFR1-4, PDGFR, Kit (c-Kit), RET (c-RET), and shows potent antitumor activities. Phase 3.	Nature, 2025, 10.1038/s41586-025-08585-z Drug Resist Updat, 2025, 81:101224 Nat Commun, 2025, 16(1):6451
S2730	Crenolanib	Crenolanib is a potent and selective inhibitor of PDGFRα/β with Kd of 2.1 nM/3.2 nM in CHO cells, also potently inhibits FLT3, sensitive to D842V mutation not V561D mutation, >100-fold more selective for PDGFR than c-Kit, VEGFR-2, TIE-2, FGFR-2, EGFR, erbB2, and Src. This compound helps to induce mitophagy.	Cancer Cell, 2025, S1535-6108(25)00070-4 Nat Commun, 2025, 16(1):1358 J Extracell Vesicles, 2025, 14(9):e70163
S1111	Foretinib	Foretinib is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met (c-Met) and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit (c-Kit), PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	J Microbiol, 2025, 63(2):e2409001 Int J Mol Sci, 2023, 24(1)757 Biol Open, 2023, 12(8)bio059994
S3012	Pazopanib	Pazopanib (GW786034) is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFR, FGFR, c-Kit and c-Fms/CSF1R with IC50 of 10 nM, 30 nM, 47 nM, 84 nM, 74 nM, 140 nM and 146 nM in cell-free assays, respectively. This compound induces cathepsin B activation and autophagy.	Nucleic Acids Res, 2025, 53(4)gkaf107 Commun Biol, 2025, 8(1):1185 Sci Rep, 2025, 15(1):35889
S1017	Cediranib (AZD2171)	Cediranib (AZD2171, NSC-732208) is a highly potent VEGFR(KDR) inhibitor with IC50 of <1 nM, also inhibits Flt1/4 with IC50 of 5 nM/≤3 nM, and shows similar activity against c-Kit and PDGFRβ. It is 36-, 110-fold and >1000-fold more selective for VEGFR than PDGFR-α, CSF-1R and Flt3 in HUVEC cells. This compound induces autophagic vacuole accumulation and is in Phase 3.	Front Oncol, 2024, 14:1302850 Cell Oncol (Dordr), 2023, 46(2):391-407 Cell Oncol (Dordr), 2023, 46(2):391-407
S1035	Pazopanib HCl	Pazopanib HCl is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFR, FGFR, c-Kit and c-Fms with IC50 of 10 nM, 30 nM, 47 nM, 84 nM, 74 nM, 140 nM and 146 nM in cell-free assays, respectively. Pazopanib induces autophagic Type II cell death.	iScience, 2024, 27(10):110862 iScience, 2023, 26(7):107116 NPJ Breast Cancer, 2022, 8(1):44
S1018	Dovitinib (TKI-258)	Dovitinib (TKI-258, CHIR258) is a multitargeted RTK inhibitor, primarily targeting class III RTKs (FLT3/c-Kit) with IC50 values of 1 nM/2 nM. It is also potent against class IV (FGFR1/3) and class V (VEGFR1-4) RTKs, exhibiting IC50 values of 8–13 nM, while showing lower potency toward InsR, EGFR, c-Met, EphA2, Tie2, IGF-1R, and HER2 in cell-free assays. Phase 4.	Spectrochim Acta A Mol Biomol Spectrosc, 2025, 343:126602 Biomed Pharmacother, 2024, 180:117533 Sci Rep, 2023, 13(1):20223
S8064	Midostaurin (PKC412)	Midostaurin is a multi-targeted kinase inhibitor, including PKCα/β/γ, Syk, Flk-1, Akt, PKA, c-Kit, c-Fgr, c-Src, FLT3, PDFRβ and VEGFR1/2 with IC50 ranging from 80-500 nM.	Blood Adv, 2025, bloodadvances.2024015427 Onco Targets Ther, 2025, 18:489-501 Blood Cancer J, 2024, 14(1):207
S5077	Regorafenib (BAY-734506) Monohydrate	Regorafenib (BAY-734506, Fluoro-sorafenib, Resihance, Stivarga, regorafaenib monohydrate) Monohydrate is a novel oral multikinase inhibitor with IC50 values of 13, 4.2, 46, 22, 7, 1.5, 2.5, 28, 19 nM for VEGFR1, murine VEGFR2, murine VEGFR3, PDGFR-β, Kit (c-Kit), RET (c-RET), RAF-1, B-RAF and B-RAF(V600E) respectively.	Nature, 2024, 629(8011):450-457 iScience, 2024, 27(10):110862 STAR Protoc, 2024, 5(2):103090
S1064	Masitinib	Masitinib is a novel inhibitor for Kit (c-Kit) and PDGFRα/β with IC50 of 200 nM and 540 nM/800 nM, weak inhibition to ABL and c-Fms. Phase 3.	Cancer Res, 2025, 10.1158/0008-5472.CAN-24-2220 iScience, 2024, 27(10):110862 bioRxiv, 2024, 2023.11.21.568071
S1207	Tivozanib	Tivozanib is a potent and selective VEGFR inhibitor for VEGFR1/2/3 with IC50 of 30 nM/6.5 nM/15 nM, and also inhibits PDGFR and c-Kit, low activity observed against FGFR-1, Flt3, c-Met, EGFR and IGF-1R. Phase 3.	bioRxiv, 2025, 2025.01.24.634732 Nat Commun, 2024, 15(1):4758 Nat Commun, 2024, 15(1):4758
S8401	Erdafitinib (JNJ-42756493)	Erdafitinib is a potent and selective orally bioavailable, pan fibroblast growth factor receptor (FGFR) inhibitor with potential antineoplastic activity. This compound also binds to RET (c-RET), CSF-1R, PDGFR-α/PDGFR-β, FLT4, Kit (c-Kit) and VEGFR-2 and induces cellular apoptosis.	Commun Biol, 2025, 8(1):394 Int J Mol Sci, 2025, 26(8)3525 J Clin Invest, 2024, 134(2)e169241
S1003	Linifanib (ABT-869)	Linifanib (ABT-869, AL39324, RG3635) is a novel, potent ATP-competitive VEGFR/PDGFR inhibitor for KDR, CSF-1R, Flt-1/3 and PDGFRβ with IC50 of 4 nM, 3 nM, 3 nM/4 nM and 66 nM respectively, mostly effective in mutant kinase-dependent cancer cells (i.e. FLT3). This compound induces autophagy and apoptosis, and is in Phase 3.	Biomed Pharmacother, 2024, 180:117533 Cell Death Discov, 2023, 9(1):57 Cell Death Discov, 2023, 9(1):57
S7765	Dovitinib (TKI258) Lactate monohydrate	Dovitinib (TKI258) Lactate monohydrate is the Lactate of Dovitinib, which is a multitargeted RTK inhibitor, mostly for class III (FLT3/c-Kit) with IC50 of 1 nM/2 nM, also potent to class IV (FGFR1/3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGFR1 and HER2. Phase 4.	Mol Cell, 2021, S1097-2765(21)00507-4 Acta Neuropathol, 2021, 10.1007/s00401-021-02327-x Cancer Res, 2021, canres.1780.2020
S5240	Lenvatinib Mesylate	Lenvatinib Mesylate is a synthetic, orally available tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR1-3), fibroblast growth factor receptor (FGFR1-4), platelet-derived growth factor receptor α (PDGFRα), stem cell factor receptor (Kit (c-Kit)), and rearranged during transfection (RET (c-RET)). This compound has potential antineoplastic activity.	Nat Commun, 2024, 15(1):1754 iScience, 2024, 27(10):110862 J Hepatocell Carcinoma, 2023, 10:697-712
S1536	CP-673451	CP-673451 is a selective inhibitor of PDGFRα/β with IC50 of 10 nM/1 nM in cell-free assays, exhibits >450-fold selectivity over other angiogenic receptors, has antiangiogenic and antitumor activity.	Nat Biotechnol, 2025, 10.1038/s41587-025-02833-3 Cancer Res, 2025, 10.1158/0008-5472.CAN-24-2220 Cell Rep Med, 2024, S2666-3791(24)00201-5
S1470	Orantinib (SU6668)	Orantinib (SU6668) has greatest potency against PDGFR autophosphorylation with Ki of 8 nM in a cell-free assay, but also strongly inhibits Flk-1 and FGFR1 trans-phosphorylation. It shows little activity against IGF-1R, Met, Src, Lck, Zap70, Abl and CDK2, and does not inhibit EGFR. This compound is in Phase 3.	bioRxiv, 2023, 2023.05.11.540170 bioRxiv, 2023, 2023.05.11.540170 J Pers Med, 2022, 12(2)258
S4947	Regorafenib Hydrochloride	Regorafenib (Stivarga, BAY 73-4506) Hydrochloride is a multi-target inhibitor for VEGFR1, Murine VEGFR2/3, PDGFRβ, Kit (c-Kit), RET (c-RET) and Raf-1 with IC50 of 13 nM, 4.2 nM/46 nM, 22 nM, 7 nM, 1.5 nM and 2.5 nM, respectively.	Cancers (Basel), 2023, 15(18)4477 Cancers (Basel), 2023, 15(18)4477 J Clin Med, 2023, 12(23)7267
S1363	Ki8751	Ki8751 is a potent and selective inhibitor of VEGFR2 with IC50 of 0.9 nM, >40-fold selective for VEGFR2 than c-Kit, PDGFRα and FGFR-2, little activity to EGFR, HGFR and InsR.	Elife, 2025, 13RP98612 Nat Commun, 2024, 15(1):2539 Drug Des Devel Ther, 2023, 17:1567-1582
S1244	Amuvatinib (MP-470)	Amuvatinib (MP-470, HPK 56) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. It suppresses c-MET and c-RET, and is also active as a DNA repair protein Rad51 inhibitor with antineoplastic activity. Phase 2.	Cancer Res, 2025, 10.1158/0008-5472.CAN-24-2220 Hematol Oncol, 2025, 43(5):e70131 bioRxiv, 2024, 2023.11.21.568071
S5234	Nintedanib Ethanesulfonate Salt	Nintedanib (Intedanib, BIBF 1120) is a small molecule tyrosine-kinase inhibitor with IC50 of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β, respectively.	iScience, 2024, 27(10):110862 Am J Cancer Res, 2023, 13(2):355-378 Theranostics, 2022, 12(2):747-766
S7667	SU5402	SU5402 is a potent multi-targeted receptor tyrosine kinase inhibitor with IC50 of 20 nM, 30 nM, and 510 nM for VEGFR2, FGFR1, and PDGF-Rβ, respectively.	Int J Mol Sci, 2025, 26(8)3536 Basic Clin Pharmacol Toxicol, 2025, 136(5):e70022 Sci Adv, 2025, 11(30):eadi2370
S8024	Tyrphostin AG 1296	Tyrphostin AG 1296 is an inhibitor of PDGFR with IC50 of 0.3-0.5 μM, no activity to EGFR. Tyrphostin AG1296 inhibits FGFR and c-Kit with IC50 of 12.3 μM and 1.8 μM in Swiss 3T3 cells. Tyrphostin AG1296 induces dramatic apoptosis in A375R cells.	Dev Cell, 2022, 57(12):1466-1481.e6 Front Pharmacol, 2021, 12:804327 Mol Med Rep, 2021, 23(4):1
S1032	Motesanib Diphosphate (AMG-706)	Motesanib Diphosphate (AMG-706) is a potent ATP-competitive inhibitor of VEGFR1/2/3 with IC50 of 2 nM/3 nM/6 nM, respectively. It shows similar activity against Kit (c-Kit) and is ~10-fold more selective for VEGFR than PDGFR and Ret. This compound is in Phase 3.	Front Cell Dev Biol, 2022, 10:836179 J Pharm Sci, 2022, 111(8):2180-2190 Drug Metab Dispos, 2021, 49(1):53-61
S8553	Avapritinib (BLU-285)	Avapritinib (BLU-285) is a small molecule kinase inhibitor that potently inhibits PDGFRα D842V mutant activity in vitro (IC50 = 0.5 nM) and PDGFRα D842V autophosphorylation in the cellular setting (IC50 = 30 nM). It is also a potent inhibitor of the analogous Kit (c-Kit) mutation, D816V in Kit (c-Kit) Exon 17 (IC50 = 0.5 nM).	Cancer Cell, 2025, S1535-6108(25)00070-4 Sci Rep, 2024, 14(1):7204 Curr Drug Metab, 2024, 25(3):197-204
S1181	ENMD-2076	ENMD-2076 has selective activity against Aurora A and Flt3 with IC50 of 14 nM and 1.86 nM, 25-fold selective for Aurora A than over Aurora B and less potent to RET, SRC, NTRK1/TRKA, CSF1R/FMS, VEGFR2/KDR, FGFR and PDGFRα. This compound inhibits the growth of a wide range of human solid tumor and hematopoietic cancer cell lines with IC50 from 0.025 to 0.7 μM, which induces apoptosis and G2/M phase arrest. Phase 2.	Int J Biol Macromol, 2025, 292:139119 Cell, 2021, 184(2):334-351.e20 Sci Adv, 2021, 7(4)eabd7851
S4736	Trapidil	Trapidil (Rocornal, Trapymin, Avantrin, Trapymine) is a PDGF antagonist that can inhibit the proliferation of the PDGF-producing glioma cells.	J Immunother Cancer, 2024, 12(11)e009805 J Pers Med, 2022, 12(2)258 Hum Cell, 2022, 10.1007/s13577-022-00671-y
S8757	Ripretinib	Ripretinib is an orally bioavailable switch pocket control inhibitor of wild-type and mutated forms of the tumor-associated antigens (TAA) mast/stem cell factor receptor (SCFR) Kit (c-Kit) and PDGFR-alpha, with IC50 values of 4 nM, 8 nM, 18 nM, 5 nM and 14 nM for WT Kit (c-Kit), V654A Kit (c-Kit), T670I Kit (c-Kit), D816H Kit (c-Kit) and D816V Kit (c-Kit), respectively.	Nature, 2024, 629(8011):450-457 Nature, 2024, 629(8011):450-457 Cell Rep Med, 2024, S2666-3791(24)00201-5
S2622	PP121	PP-121 is a multi-targeted inhibitor of PDGFR, Hck, mTOR, VEGFR2, Src and Abl with IC50 of 2 nM, 8 nM, 10 nM, 12 nM, 14 nM and 18 nM, also inhibits DNA-PK with IC50 of 60 nM.	Life Sci Alliance, 2021, 4(2)e202000882 PLoS One, 2016, 11(10):e0164895 PLoS One, 2016, 11(10):e0164895
S8015	Agerafenib (CEP-32496)	Agerafenib (CEP-32496) is a highly potent inhibitor of BRAF(V600E/WT) and c-Raf with Kd of 14 nM/36 nM and 39 nM, respectively. It also shows potent activity against Abl-1, c-Kit, Ret (c-Ret), PDGFRβ and VEGFR2, but has insignificant affinity for MEK-1, MEK-2, ERK-1 and ERK-2. This compound is currently in Phase 1/2 clinical trials.	Mol Pharmacol, 2021, 99(6):435-447 Dis Model Mech, 2020, dmm.047779 Cancer Immunol Res, 2019,
S2231	Telatinib	Telatinib (BAY 57-9352) is a potent inhibitor of VEGFR2/3, c-Kit and PDGFRα with IC50 of 6 nM/4 nM, 1 nM and 15 nM, respectively. Phase 2.	Sci Adv, 2022, 8(6):eabg9455 Leiden University Scholarly Publications, 2020, N/A Cell Stem Cell, 2019, 24(4):654-669
S2774	MK-2461	MK-2461 is a potent, multi-targeted inhibitor for c-Met(WT/mutants) with IC50 of 0.4-2.5 nM, less potent to Ron, Flt1; 8- to 30-fold greater selectivity of c-Met targets versus FGFR1, FGFR2, FGFR3, PDGFRβ, KDR, Flt3, Flt4, TrkA, and TrkB. Phase 1/2.	Mol Carcinog, 2021, 60(7):481-496 G3 (Bethesda), 2021, 11(10)jkab265 Mol Cell Biochem, 2018, 449(1-2):1-8
S7003	AZD2932	AZD2932 is a potent and mutil-targeted protein tyrosine kinase inhibitor with IC50 of 8 nM, 4 nM, 7 nM, and 9 nM for VEGFR-2, PDGFRβ, Flt-3, and c-Kit, respectively.	Cancer Res, 2020, canres.1992.2020 Molecules, 2020, 8;25(9) pii: E2220 Development, 2016, 143(23):4394-4404
S0504	SU14813	SU14813 (SU 014813) is a multiple receptor tyrosine kinase inhibitor with IC50 of 50 nM, 2 nM, 4 nM and 15 nM for VEGFR2, VEGFR1, PDGFRβ and Kit (c-Kit). This compound exhibits potent antiangiogenic and antitumor activity.	Cancer Cell, 2022, S1535-6108(22)00312-9 Adv Sci (Weinh), 2021, e2101848
S8721	PDGFR inhibitor 1	PDGFR inhibitor 1 is an orally bioavailable switch pocket control inhibitor of wild-type and mutated forms of Kit (c-Kit) and PDGFR with potential antineoplastic activity. It also inhibits several other kinases, including VEGFR2, TIE2, PDGFR-beta and CSF1R, thereby further inhibiting tumor cell growth.	bioRxiv, 2025, 2025.06.11.659120 Elife, 2023, 12e79840 Elife, 2023, 12e79840
S6526	SKLB 610	SKLB-610 is a multi-target inhibitor of the tyrosine kinases. It is most potent against VEGFR2 and exhibits slightly weaker inhibitor of FGFR2 and PDGFR.	Biomed Pharmacother, 2022, 149:112922 Int J Mol Sci, 2022, 23(14)7853
S8161	ON123300	ON123300 is a potent and multi-targeted kinase inhibitor with IC50 of 3.9 nM, 5 nM, 26 nM, 26 nM, 9.2 nM and 11nM for CDK4, Ark5/NUAK1, PDGFRβ, FGFR1, RET (c-RET), and Fyn, respectively.	Cell Rep Med, 2025, S2666-3791(25)00231-9 Cell Rep, 2024, 43(7):114446 J Cell Sci, 2021, jcs.258685
S2895	Tyrphostin 9	Tyrphostin 9 (SF 6847, RG-50872) is firstly designed as an EGFR inhibitor with IC50 of 460 μM, but is also found to be more potent to PDGFR with IC50 of 0.5 μM.	Cell Rep, 2022, 38(10):110475
E4449	AG 825	AG-825 (Tyrphostin AG-825) is a potent and selective inhibitor of ErbB2 with IC50 values of 0.15 µM. It also inhibits PDGFR autophosphorylation with IC50 value of 40 µM. It exhibits anti-cancer activity and significantly induces apoptosis in cancer cells.
S7688	Ki20227	Ki20227 is an orally active and highly selective inhibitor of c-Fms tyrosine kinase(CSF1R) with IC50 of 2 nM, 12 nM, 451 nM and 217 nM for c-Fms, vascular endothelial growth factor receptor-2 (KDR/VEGFR-2), stem cell factor receptor (c-Kit), and platelet-derived growth factor receptor beta (PDGFRβ), respectively.	Cancer Immunol Immunother, 2024, 73(5):76 Cancer Immunol Immunother, 2024, 73(5):76
S5272	Toceranib phosphate	Toceranib phosphate (Palladia, SU11654), the phosphate salt of toceranib, is a selective inhibitor of the tyrosine kinase activity of several members of the split kinase RTK family, including Flk-1/KDR, PDGFR, and Kit with Ki values of 6 nM and 5 nM for Flk-1/KDR and PDGFRβ, respectively.	Front Vet Sci, 2024, 11:1392728
S4018	Sennoside B	Sennoside B, a kind of irritant laxative isolated from rhei rhizome, inhibits PDGF-stimulated cell proliferation.
S0763	Tyrphostin AG1433	Tyrphostin AG1433 (AG1433, SU1433) is a selective platelet-derived growth factor receptor β (PDGFRβ) and vascular endothelial growth factor receptor 2 (VEGFR-2, Flk-1/KDR) inhibitor with IC50s of 5.0 μM and 9.3 μM, respectively.
E0616	Chiauranib	Chiauranib (CS2164) selectively inhibits multiple kinase targets aurora B kinase (AURKB), colony-stimulating factor 1 receptor (CSF1R), and vascular endothelial growth factor receptor (VEGFR)/platelet-derived growth factor receptor (PDGFR)/c-Kit , thereby inhibiting the rapid proliferation of tumor cells, enhancing the antitumor immunity, and inhibiting tumor angiogenesis, to achieve the anti-tumor efficacy.
E2828	AG 1295	AG 1295 is a selective and specific inhibitor of platelet-derived growth factor receptor (PDGFR) tyrosine-kinase. It inhibits PDGFR autophosphorylation with IC50 values of 0.3-0.5 μM in membrane autophosphorylation assays, respectively.
S6843	Vorolanib	Vorolanib (X-82,CM082) is an oral, multikinase, dual inhibitor of vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) with antiangiogenic and antineoplastic activities.
E0814	Masitinib mesylate	Masitinib mesylate (AB-1010 mesylate) is a potent, orally bioavailable, and selective inhibitor of c-Kit with IC50 of 200 nM for human recombinant c-Kit, also inhibits PDGFRα/β with IC50s of 540/800 nM, Lyn with IC50 of 510 nM for LynB, and, to a lesser extent, FGFR3 and FAK.
S8780	AZD3229	AZD3229 is a potent, pan-Kit (c-Kit) mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant Kit (c-Kit) driven Ba/F3 cell lines (GI50=1-50 nM), with good margin to KDR-driven effects. It also inhibits PDGFR mutants (Tel-PDGFRα, Tel-PDGFRβ, V561D/D842V).
E2548	N-(p-Coumaroyl) Serotonin	N-(p-Coumaroyl) Serotonin (p-coumaroylserotonin) is a polyphenol isolated from the seeds of safflower and has antioxidative, anti-atherogenic and anti-inflammatory properties, can inhibits PDGF-induced on phosphorylation of PDGF receptor and Ca2+ release from sarcoplasmic reticulum.
E0050	Seralutinib (GB002)	Seralutinib (PK10571, GB002) is a novel PDGFR kinase inhibitor with IC50s of 8 nM and 10 nM for PDGFRα and PDGFRβ in enzyme assays, respectively.
E2393	JNJ-10198409	JNJ-10198409, a relatively selective, orally active, and ATP competitive PDGF-RTK (platelet-derived growth factor receptor tyrosine kinase) inhibitor with IC50 of 2 nM, is a dual-mechanism, antiangiogenic, and tumor cell antiproliferative agent, has good activity against PDGFRβ kinase and PDGFRα kinase with IC50 of 4.2 and 45 nM, respectively.
S9973	Flumatinib (HH-GV-678)	Flumatinib (HH-GV-678) is a novel inhibitor of Bcr-Abl with IC50 values of 1.2  nM, 307.6  nM and 665.5  nM for c-Abl, PDGFRβand c-Kit, respectively.
S7397	Sorafenib (BAY 43-9006)	Sorafenib is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. Sorafenib inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. Sorafenib induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Mol Cancer, 2025, 24(1):34 Nat Commun, 2025, 16(1):509 Adv Sci (Weinh), 2025, 12(30):e04372
S2475	Imatinib	Imatinib is a multi-target inhibitor of tyrosine kinase with inhibition for v-Abl, c-Kit and PDGFR, IC50 values are 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively. Imatinib (STI571) induces autophagy.	Cancer Cell, 2025, 43(4):776-796.e14 Theranostics, 2025, 15(8):3589-3609 Genome Med, 2025, 17(1):14
S1040	Sorafenib tosylate	Sorafenib tosylate is a multikinase inhibitor of Raf-1 and B-Raf with IC50 of 6 nM and 22 nM in cell-free assays, respectively. This compound inhibits VEGFR-2, VEGFR-3, PDGFR-β, Flt-3 and c-KIT with IC50 of 90 nM, 20 nM, 57 nM, 59 nM and 68 nM, respectively. It induces autophagy and apoptosis and activates ferroptosis with anti-tumor activity.	Int J Oncol, 2025, 67(3)72 Nature, 2024, 629(8013):927-936 Cell Mol Life Sci, 2024, 81(1):238
S1026	Imatinib (STI571) Mesylate	Imatinib Mesylate is an orally bioavailability mesylate salt of Imatinib, which is a multi-target inhibitor of v-Abl, c-Kit and PDGFR with IC50 of 0.6 μM, 0.1 μM and 0.1 μM in cell-free or cell-based assays, respectively. Imatinib Mesylate (STI571) induces autophagy.	Sci Immunol, 2025, 10(109):eads5818 Blood Adv, 2025, bloodadvances.2024015364 Eur J Med Chem, 2025, 284:117211
S7781	Sunitinib (SU-11248)	Sunitinib is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM, and also inhibits c-Kit. Sunitinib is also a dose-dependent inhibitor of the autophosphorylation activity of IRE1α. Sunitinib induces autophagy and apoptosis.	Cancer Cell, 2025, 43(4):776-796.e14 Mol Cancer, 2025, 24(1):179 J Exp Clin Cancer Res, 2025, 44(1):290
S1490	Ponatinib (AP24534)	Ponatinib is a novel, potent multi-target inhibitor of Abl, PDGFRα, VEGFR2, FGFR1 and Src with IC50 of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM and 5.4 nM in cell-free assays, respectively. Ponatinib (AP24534) inhibits autophagy.	Nat Commun, 2025, 16(1):471 Theranostics, 2025, 15(8):3589-3609 J Exp Clin Cancer Res, 2025, 44(1):290
S1178	Regorafenib (BAY 73-4506)	Regorafenib is a multi-target inhibitor for VEGFR1, VEGFR2, VEGFR3, PDGFRβ, Kit (c-Kit), RET (c-RET) and Raf-1 with IC50 of 13 nM/4.2 nM/46 nM, 22 nM, 7 nM, 1.5 nM and 2.5 nM in cell-free assays, respectively. Regorafenib induces autophagy.	Nat Commun, 2025, 16(1):509 Cell Death Differ, 2025, 10.1038/s41418-025-01536-1 Cell Mol Gastroenterol Hepatol, 2025, S2352-345X(25)00026-8
S1005	Axitinib (AG-013736)	Axitinib is a multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFRβ and c-Kit with IC50 of 0.1 nM, 0.2 nM, 0.1-0.3 nM, 1.6 nM and 1.7 nM in Porcine aorta endothelial cells, respectively.	Cancer Cell, 2025, S1535-6108(25)00070-4 Chem Biol Interact, 2025, 418:111628 Development, 2025, 152(13)dev204684
S1042	Sunitinib malate	Sunitinib malate is a multi-targeted RTK inhibitor targeting VEGFR2 (Flk-1) and PDGFRβ with IC50 of 80 nM and 2 nM in cell-free assays, and also inhibits c-Kit. Sunitinib Malate effectively inhibits autophosphorylation of Ire1α. Sunitinib Malate increases both death receptor and mitochondrial-dependent apoptosis.	CNS Neurosci Ther, 2025, 31(12):e70696 Sci Rep, 2025, 15(1):35889 Cell Oncol (Dordr), 2024, 10.1007/s13402-024-00939-5
S1010	Nintedanib (BIBF 1120)	Nintedanib is a potent triple angiokinase inhibitor for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β with IC50 of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM in cell-free assays. Phase 3.	Nat Commun, 2025, 16(1):471 Cell Death Dis, 2025, 16(1):196 Eur J Pharmacol, 2025, 1005:178058
S1164	Lenvatinib (E7080)	Lenvatinib is a multi-target inhibitor, mostly for VEGFR2(KDR)/VEGFR3(Flt-4) with IC50 of 4 nM/5.2 nM, less potent against VEGFR1/Flt-1, ~10-fold more selective for VEGFR2/3 against FGFR1, PDGFRα/β in cell-free assays. This compound also inhibits FGFR1-4, PDGFR, Kit (c-Kit), RET (c-RET), and shows potent antitumor activities. Phase 3.	Nature, 2025, 10.1038/s41586-025-08585-z Drug Resist Updat, 2025, 81:101224 Nat Commun, 2025, 16(1):6451
S2730	Crenolanib	Crenolanib is a potent and selective inhibitor of PDGFRα/β with Kd of 2.1 nM/3.2 nM in CHO cells, also potently inhibits FLT3, sensitive to D842V mutation not V561D mutation, >100-fold more selective for PDGFR than c-Kit, VEGFR-2, TIE-2, FGFR-2, EGFR, erbB2, and Src. This compound helps to induce mitophagy.	Cancer Cell, 2025, S1535-6108(25)00070-4 Nat Commun, 2025, 16(1):1358 J Extracell Vesicles, 2025, 14(9):e70163
S1111	Foretinib	Foretinib is an ATP-competitive inhibitor of HGFR and VEGFR, mostly for Met (c-Met) and KDR with IC50 of 0.4 nM and 0.9 nM in cell-free assays. Less potent against Ron, Flt-1/3/4, Kit (c-Kit), PDGFRα/β and Tie-2, and little activity to FGFR1 and EGFR. Phase 2.	J Microbiol, 2025, 63(2):e2409001 Int J Mol Sci, 2023, 24(1)757 Biol Open, 2023, 12(8)bio059994
S3012	Pazopanib	Pazopanib (GW786034) is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFR, FGFR, c-Kit and c-Fms/CSF1R with IC50 of 10 nM, 30 nM, 47 nM, 84 nM, 74 nM, 140 nM and 146 nM in cell-free assays, respectively. This compound induces cathepsin B activation and autophagy.	Nucleic Acids Res, 2025, 53(4)gkaf107 Commun Biol, 2025, 8(1):1185 Sci Rep, 2025, 15(1):35889
S1017	Cediranib (AZD2171)	Cediranib (AZD2171, NSC-732208) is a highly potent VEGFR(KDR) inhibitor with IC50 of <1 nM, also inhibits Flt1/4 with IC50 of 5 nM/≤3 nM, and shows similar activity against c-Kit and PDGFRβ. It is 36-, 110-fold and >1000-fold more selective for VEGFR than PDGFR-α, CSF-1R and Flt3 in HUVEC cells. This compound induces autophagic vacuole accumulation and is in Phase 3.	Front Oncol, 2024, 14:1302850 Cell Oncol (Dordr), 2023, 46(2):391-407 Cell Oncol (Dordr), 2023, 46(2):391-407
S1035	Pazopanib HCl	Pazopanib HCl is a novel multi-target inhibitor of VEGFR1, VEGFR2, VEGFR3, PDGFR, FGFR, c-Kit and c-Fms with IC50 of 10 nM, 30 nM, 47 nM, 84 nM, 74 nM, 140 nM and 146 nM in cell-free assays, respectively. Pazopanib induces autophagic Type II cell death.	iScience, 2024, 27(10):110862 iScience, 2023, 26(7):107116 NPJ Breast Cancer, 2022, 8(1):44
S1018	Dovitinib (TKI-258)	Dovitinib (TKI-258, CHIR258) is a multitargeted RTK inhibitor, primarily targeting class III RTKs (FLT3/c-Kit) with IC50 values of 1 nM/2 nM. It is also potent against class IV (FGFR1/3) and class V (VEGFR1-4) RTKs, exhibiting IC50 values of 8–13 nM, while showing lower potency toward InsR, EGFR, c-Met, EphA2, Tie2, IGF-1R, and HER2 in cell-free assays. Phase 4.	Spectrochim Acta A Mol Biomol Spectrosc, 2025, 343:126602 Biomed Pharmacother, 2024, 180:117533 Sci Rep, 2023, 13(1):20223
S8064	Midostaurin (PKC412)	Midostaurin is a multi-targeted kinase inhibitor, including PKCα/β/γ, Syk, Flk-1, Akt, PKA, c-Kit, c-Fgr, c-Src, FLT3, PDFRβ and VEGFR1/2 with IC50 ranging from 80-500 nM.	Blood Adv, 2025, bloodadvances.2024015427 Onco Targets Ther, 2025, 18:489-501 Blood Cancer J, 2024, 14(1):207
S5077	Regorafenib (BAY-734506) Monohydrate	Regorafenib (BAY-734506, Fluoro-sorafenib, Resihance, Stivarga, regorafaenib monohydrate) Monohydrate is a novel oral multikinase inhibitor with IC50 values of 13, 4.2, 46, 22, 7, 1.5, 2.5, 28, 19 nM for VEGFR1, murine VEGFR2, murine VEGFR3, PDGFR-β, Kit (c-Kit), RET (c-RET), RAF-1, B-RAF and B-RAF(V600E) respectively.	Nature, 2024, 629(8011):450-457 iScience, 2024, 27(10):110862 STAR Protoc, 2024, 5(2):103090
S1064	Masitinib	Masitinib is a novel inhibitor for Kit (c-Kit) and PDGFRα/β with IC50 of 200 nM and 540 nM/800 nM, weak inhibition to ABL and c-Fms. Phase 3.	Cancer Res, 2025, 10.1158/0008-5472.CAN-24-2220 iScience, 2024, 27(10):110862 bioRxiv, 2024, 2023.11.21.568071
S1207	Tivozanib	Tivozanib is a potent and selective VEGFR inhibitor for VEGFR1/2/3 with IC50 of 30 nM/6.5 nM/15 nM, and also inhibits PDGFR and c-Kit, low activity observed against FGFR-1, Flt3, c-Met, EGFR and IGF-1R. Phase 3.	bioRxiv, 2025, 2025.01.24.634732 Nat Commun, 2024, 15(1):4758 Nat Commun, 2024, 15(1):4758
S8401	Erdafitinib (JNJ-42756493)	Erdafitinib is a potent and selective orally bioavailable, pan fibroblast growth factor receptor (FGFR) inhibitor with potential antineoplastic activity. This compound also binds to RET (c-RET), CSF-1R, PDGFR-α/PDGFR-β, FLT4, Kit (c-Kit) and VEGFR-2 and induces cellular apoptosis.	Commun Biol, 2025, 8(1):394 Int J Mol Sci, 2025, 26(8)3525 J Clin Invest, 2024, 134(2)e169241
S1003	Linifanib (ABT-869)	Linifanib (ABT-869, AL39324, RG3635) is a novel, potent ATP-competitive VEGFR/PDGFR inhibitor for KDR, CSF-1R, Flt-1/3 and PDGFRβ with IC50 of 4 nM, 3 nM, 3 nM/4 nM and 66 nM respectively, mostly effective in mutant kinase-dependent cancer cells (i.e. FLT3). This compound induces autophagy and apoptosis, and is in Phase 3.	Biomed Pharmacother, 2024, 180:117533 Cell Death Discov, 2023, 9(1):57 Cell Death Discov, 2023, 9(1):57
S7765	Dovitinib (TKI258) Lactate monohydrate	Dovitinib (TKI258) Lactate monohydrate is the Lactate of Dovitinib, which is a multitargeted RTK inhibitor, mostly for class III (FLT3/c-Kit) with IC50 of 1 nM/2 nM, also potent to class IV (FGFR1/3) and class V (VEGFR1-4) RTKs with IC50 of 8-13 nM, less potent to InsR, EGFR, c-Met, EphA2, Tie2, IGFR1 and HER2. Phase 4.	Mol Cell, 2021, S1097-2765(21)00507-4 Acta Neuropathol, 2021, 10.1007/s00401-021-02327-x Cancer Res, 2021, canres.1780.2020
S5240	Lenvatinib Mesylate	Lenvatinib Mesylate is a synthetic, orally available tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor (VEGFR1-3), fibroblast growth factor receptor (FGFR1-4), platelet-derived growth factor receptor α (PDGFRα), stem cell factor receptor (Kit (c-Kit)), and rearranged during transfection (RET (c-RET)). This compound has potential antineoplastic activity.	Nat Commun, 2024, 15(1):1754 iScience, 2024, 27(10):110862 J Hepatocell Carcinoma, 2023, 10:697-712
S1536	CP-673451	CP-673451 is a selective inhibitor of PDGFRα/β with IC50 of 10 nM/1 nM in cell-free assays, exhibits >450-fold selectivity over other angiogenic receptors, has antiangiogenic and antitumor activity.	Nat Biotechnol, 2025, 10.1038/s41587-025-02833-3 Cancer Res, 2025, 10.1158/0008-5472.CAN-24-2220 Cell Rep Med, 2024, S2666-3791(24)00201-5
S1470	Orantinib (SU6668)	Orantinib (SU6668) has greatest potency against PDGFR autophosphorylation with Ki of 8 nM in a cell-free assay, but also strongly inhibits Flk-1 and FGFR1 trans-phosphorylation. It shows little activity against IGF-1R, Met, Src, Lck, Zap70, Abl and CDK2, and does not inhibit EGFR. This compound is in Phase 3.	bioRxiv, 2023, 2023.05.11.540170 bioRxiv, 2023, 2023.05.11.540170 J Pers Med, 2022, 12(2)258
S4947	Regorafenib Hydrochloride	Regorafenib (Stivarga, BAY 73-4506) Hydrochloride is a multi-target inhibitor for VEGFR1, Murine VEGFR2/3, PDGFRβ, Kit (c-Kit), RET (c-RET) and Raf-1 with IC50 of 13 nM, 4.2 nM/46 nM, 22 nM, 7 nM, 1.5 nM and 2.5 nM, respectively.	Cancers (Basel), 2023, 15(18)4477 Cancers (Basel), 2023, 15(18)4477 J Clin Med, 2023, 12(23)7267
S1363	Ki8751	Ki8751 is a potent and selective inhibitor of VEGFR2 with IC50 of 0.9 nM, >40-fold selective for VEGFR2 than c-Kit, PDGFRα and FGFR-2, little activity to EGFR, HGFR and InsR.	Elife, 2025, 13RP98612 Nat Commun, 2024, 15(1):2539 Drug Des Devel Ther, 2023, 17:1567-1582
S1244	Amuvatinib (MP-470)	Amuvatinib (MP-470, HPK 56) is a potent and multi-targeted inhibitor of c-Kit, PDGFRα and Flt3 with IC50 of 10 nM, 40 nM and 81 nM, respectively. It suppresses c-MET and c-RET, and is also active as a DNA repair protein Rad51 inhibitor with antineoplastic activity. Phase 2.	Cancer Res, 2025, 10.1158/0008-5472.CAN-24-2220 Hematol Oncol, 2025, 43(5):e70131 bioRxiv, 2024, 2023.11.21.568071
S5234	Nintedanib Ethanesulfonate Salt	Nintedanib (Intedanib, BIBF 1120) is a small molecule tyrosine-kinase inhibitor with IC50 of 34 nM/13 nM/13 nM, 69 nM/37 nM/108 nM and 59 nM/65 nM for VEGFR1/2/3, FGFR1/2/3 and PDGFRα/β, respectively.	iScience, 2024, 27(10):110862 Am J Cancer Res, 2023, 13(2):355-378 Theranostics, 2022, 12(2):747-766
S7667	SU5402	SU5402 is a potent multi-targeted receptor tyrosine kinase inhibitor with IC50 of 20 nM, 30 nM, and 510 nM for VEGFR2, FGFR1, and PDGF-Rβ, respectively.	Int J Mol Sci, 2025, 26(8)3536 Basic Clin Pharmacol Toxicol, 2025, 136(5):e70022 Sci Adv, 2025, 11(30):eadi2370
S8024	Tyrphostin AG 1296	Tyrphostin AG 1296 is an inhibitor of PDGFR with IC50 of 0.3-0.5 μM, no activity to EGFR. Tyrphostin AG1296 inhibits FGFR and c-Kit with IC50 of 12.3 μM and 1.8 μM in Swiss 3T3 cells. Tyrphostin AG1296 induces dramatic apoptosis in A375R cells.	Dev Cell, 2022, 57(12):1466-1481.e6 Front Pharmacol, 2021, 12:804327 Mol Med Rep, 2021, 23(4):1
S1032	Motesanib Diphosphate (AMG-706)	Motesanib Diphosphate (AMG-706) is a potent ATP-competitive inhibitor of VEGFR1/2/3 with IC50 of 2 nM/3 nM/6 nM, respectively. It shows similar activity against Kit (c-Kit) and is ~10-fold more selective for VEGFR than PDGFR and Ret. This compound is in Phase 3.	Front Cell Dev Biol, 2022, 10:836179 J Pharm Sci, 2022, 111(8):2180-2190 Drug Metab Dispos, 2021, 49(1):53-61
S8553	Avapritinib (BLU-285)	Avapritinib (BLU-285) is a small molecule kinase inhibitor that potently inhibits PDGFRα D842V mutant activity in vitro (IC50 = 0.5 nM) and PDGFRα D842V autophosphorylation in the cellular setting (IC50 = 30 nM). It is also a potent inhibitor of the analogous Kit (c-Kit) mutation, D816V in Kit (c-Kit) Exon 17 (IC50 = 0.5 nM).	Cancer Cell, 2025, S1535-6108(25)00070-4 Sci Rep, 2024, 14(1):7204 Curr Drug Metab, 2024, 25(3):197-204
S1181	ENMD-2076	ENMD-2076 has selective activity against Aurora A and Flt3 with IC50 of 14 nM and 1.86 nM, 25-fold selective for Aurora A than over Aurora B and less potent to RET, SRC, NTRK1/TRKA, CSF1R/FMS, VEGFR2/KDR, FGFR and PDGFRα. This compound inhibits the growth of a wide range of human solid tumor and hematopoietic cancer cell lines with IC50 from 0.025 to 0.7 μM, which induces apoptosis and G2/M phase arrest. Phase 2.	Int J Biol Macromol, 2025, 292:139119 Cell, 2021, 184(2):334-351.e20 Sci Adv, 2021, 7(4)eabd7851
S8757	Ripretinib	Ripretinib is an orally bioavailable switch pocket control inhibitor of wild-type and mutated forms of the tumor-associated antigens (TAA) mast/stem cell factor receptor (SCFR) Kit (c-Kit) and PDGFR-alpha, with IC50 values of 4 nM, 8 nM, 18 nM, 5 nM and 14 nM for WT Kit (c-Kit), V654A Kit (c-Kit), T670I Kit (c-Kit), D816H Kit (c-Kit) and D816V Kit (c-Kit), respectively.	Nature, 2024, 629(8011):450-457 Nature, 2024, 629(8011):450-457 Cell Rep Med, 2024, S2666-3791(24)00201-5
S2622	PP121	PP-121 is a multi-targeted inhibitor of PDGFR, Hck, mTOR, VEGFR2, Src and Abl with IC50 of 2 nM, 8 nM, 10 nM, 12 nM, 14 nM and 18 nM, also inhibits DNA-PK with IC50 of 60 nM.	Life Sci Alliance, 2021, 4(2)e202000882 PLoS One, 2016, 11(10):e0164895 PLoS One, 2016, 11(10):e0164895
S8015	Agerafenib (CEP-32496)	Agerafenib (CEP-32496) is a highly potent inhibitor of BRAF(V600E/WT) and c-Raf with Kd of 14 nM/36 nM and 39 nM, respectively. It also shows potent activity against Abl-1, c-Kit, Ret (c-Ret), PDGFRβ and VEGFR2, but has insignificant affinity for MEK-1, MEK-2, ERK-1 and ERK-2. This compound is currently in Phase 1/2 clinical trials.	Mol Pharmacol, 2021, 99(6):435-447 Dis Model Mech, 2020, dmm.047779 Cancer Immunol Res, 2019,
S2231	Telatinib	Telatinib (BAY 57-9352) is a potent inhibitor of VEGFR2/3, c-Kit and PDGFRα with IC50 of 6 nM/4 nM, 1 nM and 15 nM, respectively. Phase 2.	Sci Adv, 2022, 8(6):eabg9455 Leiden University Scholarly Publications, 2020, N/A Cell Stem Cell, 2019, 24(4):654-669
S2774	MK-2461	MK-2461 is a potent, multi-targeted inhibitor for c-Met(WT/mutants) with IC50 of 0.4-2.5 nM, less potent to Ron, Flt1; 8- to 30-fold greater selectivity of c-Met targets versus FGFR1, FGFR2, FGFR3, PDGFRβ, KDR, Flt3, Flt4, TrkA, and TrkB. Phase 1/2.	Mol Carcinog, 2021, 60(7):481-496 G3 (Bethesda), 2021, 11(10)jkab265 Mol Cell Biochem, 2018, 449(1-2):1-8
S7003	AZD2932	AZD2932 is a potent and mutil-targeted protein tyrosine kinase inhibitor with IC50 of 8 nM, 4 nM, 7 nM, and 9 nM for VEGFR-2, PDGFRβ, Flt-3, and c-Kit, respectively.	Cancer Res, 2020, canres.1992.2020 Molecules, 2020, 8;25(9) pii: E2220 Development, 2016, 143(23):4394-4404
S0504	SU14813	SU14813 (SU 014813) is a multiple receptor tyrosine kinase inhibitor with IC50 of 50 nM, 2 nM, 4 nM and 15 nM for VEGFR2, VEGFR1, PDGFRβ and Kit (c-Kit). This compound exhibits potent antiangiogenic and antitumor activity.	Cancer Cell, 2022, S1535-6108(22)00312-9 Adv Sci (Weinh), 2021, e2101848
S8721	PDGFR inhibitor 1	PDGFR inhibitor 1 is an orally bioavailable switch pocket control inhibitor of wild-type and mutated forms of Kit (c-Kit) and PDGFR with potential antineoplastic activity. It also inhibits several other kinases, including VEGFR2, TIE2, PDGFR-beta and CSF1R, thereby further inhibiting tumor cell growth.	bioRxiv, 2025, 2025.06.11.659120 Elife, 2023, 12e79840 Elife, 2023, 12e79840
S6526	SKLB 610	SKLB-610 is a multi-target inhibitor of the tyrosine kinases. It is most potent against VEGFR2 and exhibits slightly weaker inhibitor of FGFR2 and PDGFR.	Biomed Pharmacother, 2022, 149:112922 Int J Mol Sci, 2022, 23(14)7853
S8161	ON123300	ON123300 is a potent and multi-targeted kinase inhibitor with IC50 of 3.9 nM, 5 nM, 26 nM, 26 nM, 9.2 nM and 11nM for CDK4, Ark5/NUAK1, PDGFRβ, FGFR1, RET (c-RET), and Fyn, respectively.	Cell Rep Med, 2025, S2666-3791(25)00231-9 Cell Rep, 2024, 43(7):114446 J Cell Sci, 2021, jcs.258685
S2895	Tyrphostin 9	Tyrphostin 9 (SF 6847, RG-50872) is firstly designed as an EGFR inhibitor with IC50 of 460 μM, but is also found to be more potent to PDGFR with IC50 of 0.5 μM.	Cell Rep, 2022, 38(10):110475
E4449	AG 825	AG-825 (Tyrphostin AG-825) is a potent and selective inhibitor of ErbB2 with IC50 values of 0.15 µM. It also inhibits PDGFR autophosphorylation with IC50 value of 40 µM. It exhibits anti-cancer activity and significantly induces apoptosis in cancer cells.
S7688	Ki20227	Ki20227 is an orally active and highly selective inhibitor of c-Fms tyrosine kinase(CSF1R) with IC50 of 2 nM, 12 nM, 451 nM and 217 nM for c-Fms, vascular endothelial growth factor receptor-2 (KDR/VEGFR-2), stem cell factor receptor (c-Kit), and platelet-derived growth factor receptor beta (PDGFRβ), respectively.	Cancer Immunol Immunother, 2024, 73(5):76 Cancer Immunol Immunother, 2024, 73(5):76
S5272	Toceranib phosphate	Toceranib phosphate (Palladia, SU11654), the phosphate salt of toceranib, is a selective inhibitor of the tyrosine kinase activity of several members of the split kinase RTK family, including Flk-1/KDR, PDGFR, and Kit with Ki values of 6 nM and 5 nM for Flk-1/KDR and PDGFRβ, respectively.	Front Vet Sci, 2024, 11:1392728
S4018	Sennoside B	Sennoside B, a kind of irritant laxative isolated from rhei rhizome, inhibits PDGF-stimulated cell proliferation.
S0763	Tyrphostin AG1433	Tyrphostin AG1433 (AG1433, SU1433) is a selective platelet-derived growth factor receptor β (PDGFRβ) and vascular endothelial growth factor receptor 2 (VEGFR-2, Flk-1/KDR) inhibitor with IC50s of 5.0 μM and 9.3 μM, respectively.
E0616	Chiauranib	Chiauranib (CS2164) selectively inhibits multiple kinase targets aurora B kinase (AURKB), colony-stimulating factor 1 receptor (CSF1R), and vascular endothelial growth factor receptor (VEGFR)/platelet-derived growth factor receptor (PDGFR)/c-Kit , thereby inhibiting the rapid proliferation of tumor cells, enhancing the antitumor immunity, and inhibiting tumor angiogenesis, to achieve the anti-tumor efficacy.
E2828	AG 1295	AG 1295 is a selective and specific inhibitor of platelet-derived growth factor receptor (PDGFR) tyrosine-kinase. It inhibits PDGFR autophosphorylation with IC50 values of 0.3-0.5 μM in membrane autophosphorylation assays, respectively.
S6843	Vorolanib	Vorolanib (X-82,CM082) is an oral, multikinase, dual inhibitor of vascular endothelial growth factor receptor (VEGFR) and platelet-derived growth factor receptor (PDGFR) with antiangiogenic and antineoplastic activities.
E0814	Masitinib mesylate	Masitinib mesylate (AB-1010 mesylate) is a potent, orally bioavailable, and selective inhibitor of c-Kit with IC50 of 200 nM for human recombinant c-Kit, also inhibits PDGFRα/β with IC50s of 540/800 nM, Lyn with IC50 of 510 nM for LynB, and, to a lesser extent, FGFR3 and FAK.
S8780	AZD3229	AZD3229 is a potent, pan-Kit (c-Kit) mutant inhibitor with potent single digit nM growth inhibition against a diverse panel of mutant Kit (c-Kit) driven Ba/F3 cell lines (GI50=1-50 nM), with good margin to KDR-driven effects. It also inhibits PDGFR mutants (Tel-PDGFRα, Tel-PDGFRβ, V561D/D842V).
E2548	N-(p-Coumaroyl) Serotonin	N-(p-Coumaroyl) Serotonin (p-coumaroylserotonin) is a polyphenol isolated from the seeds of safflower and has antioxidative, anti-atherogenic and anti-inflammatory properties, can inhibits PDGF-induced on phosphorylation of PDGF receptor and Ca2+ release from sarcoplasmic reticulum.
E0050	Seralutinib (GB002)	Seralutinib (PK10571, GB002) is a novel PDGFR kinase inhibitor with IC50s of 8 nM and 10 nM for PDGFRα and PDGFRβ in enzyme assays, respectively.
E2393	JNJ-10198409	JNJ-10198409, a relatively selective, orally active, and ATP competitive PDGF-RTK (platelet-derived growth factor receptor tyrosine kinase) inhibitor with IC50 of 2 nM, is a dual-mechanism, antiangiogenic, and tumor cell antiproliferative agent, has good activity against PDGFRβ kinase and PDGFRα kinase with IC50 of 4.2 and 45 nM, respectively.
S9973	Flumatinib (HH-GV-678)	Flumatinib (HH-GV-678) is a novel inhibitor of Bcr-Abl with IC50 values of 1.2  nM, 307.6  nM and 665.5  nM for c-Abl, PDGFRβand c-Kit, respectively.
S4736	Trapidil	Trapidil (Rocornal, Trapymin, Avantrin, Trapymine) is a PDGF antagonist that can inhibit the proliferation of the PDGF-producing glioma cells.	J Immunother Cancer, 2024, 12(11)e009805 J Pers Med, 2022, 12(2)258 Hum Cell, 2022, 10.1007/s13577-022-00671-y

Signaling Pathway Map

PDGFR Receptor Biology and Signaling Pathways

The PDGFR family belongs to the receptor tyrosine kinase (RTK) superfamily, characterized by an extracellular ligand-binding domain, a single transmembrane domain, and an intracellular tyrosine kinase domain. The two main isoforms, PDGFRα and PDGFRβ, are encoded by different genes and exhibit distinct expression patterns and ligand specificities. PDGFRα binds to PDGF-A, PDGF-B, and PDGF-C, while PDGFRβ primarily interacts with PDGF-B and PDGF-D. Ligand binding induces receptor dimerization (homo- or heterodimerization between PDGFRα and PDGFRβ), which activates the intracellular tyrosine kinase domain, leading to autophosphorylation of specific tyrosine residues.

PDGFR Signaling Cascade in Normal and Pathological Conditions

The phosphorylated tyrosine residues of PDGFR serve as docking sites for various downstream signaling molecules, initiating multiple intracellular pathways that regulate cellular functions. Key signaling pathways activated by PDGFR include the Ras-Raf-MEK-ERK pathway, which promotes cell proliferation and survival; the PI3K-AKT-mTOR pathway, which regulates cell metabolism and anti-apoptotic processes; and the JAK/STAT pathway, which mediates gene transcription involved in cell growth and differentiation. In normal physiological conditions, PDGFR signaling is tightly regulated, ensuring proper tissue development, wound healing, and angiogenesis. However, in pathological states such as cancer, dysregulated PDGFR signaling disrupts this balance, leading to uncontrolled cell proliferation, enhanced cell migration and invasion, and increased angiogenesis, all of which contribute to tumor growth and metastasis.

Structural Differences Between PDGFRα and PDGFRβ

Although PDGFRα and PDGFRβ share high homology in their tyrosine kinase domains (approximately 85% amino acid sequence identity), they exhibit significant differences in their extracellular ligand-binding domains and tissue expression profiles. PDGFRα is highly expressed in embryonic tissues, and in adult tissues, it is found in fibroblasts, smooth muscle cells, and certain types of stem cells. PDGFRβ, on the other hand, is predominantly expressed in vascular smooth muscle cells, pericytes, and macrophages. These structural and expression differences contribute to the distinct roles of PDGFRα and PDGFRβ in normal physiology and disease. For example, PDGFRα mutations are frequently associated with gastrointestinal stromal tumors (GISTs), while PDGFRβ overexpression is often observed in gliomas and hematological malignancies.

PDGFR Mutation and Its Role in Cancer Oncogenesis

Mutations in the PDGFR gene are a major driver of dysregulated PDGFR signaling in cancer. These mutations can occur in the extracellular ligand-binding domain, the transmembrane domain, or the intracellular tyrosine kinase domain, leading to constitutive activation of the receptor independent of ligand binding. The identification and characterization of PDGFR mutations have provided critical insights into the molecular mechanisms of cancer development and have guided the development of targeted PDGFR inhibitors.

Common PDGFR Mutations in Human Cancers

One of the most well-characterized PDGFR mutations is the c-KIT/PDGFRα mutation in GISTs. Approximately 5-10% of GISTs harbor PDGFRα mutations, with the most common being the D842V mutation in the tyrosine kinase domain. This mutation renders PDGFRα constitutively active, promoting tumor cell proliferation and survival. Other common PDGFR mutations include the V561D mutation in the extracellular domain of PDGFRα, which enhances ligand binding affinity, and the R841W mutation in the tyrosine kinase domain of PDGFRβ, which is associated with chronic myelomonocytic leukemia (CMML). In addition, PDGFR gene amplifications and translocations have also been reported in various cancers, such as lung cancer, breast cancer, and glioblastoma, leading to receptor overexpression and hyperactivation.

Mechanisms of Mutation-Driven PDGFR Activation in Cancer

PDGFR mutations drive oncogenesis primarily by inducing constitutive receptor activation. For example, mutations in the tyrosine kinase domain, such as D842V in PDGFRα, disrupt the autoinhibitory conformation of the receptor, allowing the kinase domain to remain active even in the absence of ligand. This leads to continuous autophosphorylation of the receptor and sustained activation of downstream signaling pathways. Mutations in the extracellular domain, on the other hand, may enhance ligand binding or promote receptor dimerization, leading to increased receptor activation. In addition, PDGFR mutations can also confer resistance to certain PDGFR inhibitors, highlighting the need for personalized therapeutic strategies based on the specific mutation profile of the tumor.

Development and Evaluation of PDGFR Inhibitors for Cancer Therapy

Based on the critical role of PDGFR signaling in cancer, numerous PDGFR inhibitors have been developed and evaluated in preclinical and clinical studies. These inhibitors can be classified into two main categories: multi-targeted tyrosine kinase inhibitors (TKIs) that inhibit PDGFR along with other RTKs, and selective PDGFR inhibitors that specifically target PDGFRα or PDGFRβ. The development of PDGFR inhibitors has been guided by a deep understanding of PDGFR structure, signaling pathways, and mutation profiles, with the goal of improving efficacy and reducing off-target effects.

Preclinical Evaluation of PDGFR Inhibitors

Preclinical studies play a crucial role in the development of PDGFR inhibitors, providing insights into their mechanism of action, efficacy, and safety. In vitro studies using cancer cell lines harboring PDGFR mutations or overexpression have been used to evaluate the inhibitory activity of PDGFR inhibitors on cell proliferation, migration, and survival. In vivo studies using xenograft mouse models or genetically engineered mouse models (GEMMs) of cancer have been used to assess the antitumor efficacy of PDGFR inhibitors in vivo, as well as their pharmacokinetic and pharmacodynamic properties. For example, preclinical studies have shown that imatinib, a multi-targeted TKI that inhibits PDGFRα, PDGFRβ, and c-KIT, effectively inhibits the growth of GIST cells harboring PDGFRα mutations. Similarly, sunitinib, another multi-targeted TKI, has been shown to inhibit PDGFR signaling and suppress tumor angiogenesis in various preclinical cancer models.

Clinical Trials of PDGFR Inhibitors in Cancer Patients

Numerous clinical trials have been conducted to evaluate the safety and efficacy of PDGFR inhibitors in cancer patients. Imatinib was the first PDGFR inhibitor approved for the treatment of GISTs, and it has significantly improved the prognosis of patients with GISTs harboring c-KIT or PDGFRα mutations. However, some patients develop resistance to imatinib over time, often due to secondary mutations in PDGFRα or c-KIT. This has led to the development of second-generation PDGFR inhibitors, such as regorafenib and ripretinib, which have shown efficacy in imatinib-resistant GISTs. In addition, PDGFR inhibitors have also been evaluated in other cancers, such as lung cancer, breast cancer, glioblastoma, and hematological malignancies. For example, clinical trials have shown that sunitinib is effective in the treatment of advanced renal cell carcinoma, in part by inhibiting PDGFR-mediated angiogenesis. However, the efficacy of PDGFR inhibitors varies depending on the type of cancer and the specific PDGFR mutation profile of the tumor, emphasizing the importance of biomarker-driven patient selection.

Challenges and Future Directions in PDGFR Inhibitor Research

Despite the significant progress in PDGFR inhibitor research, several challenges remain. One of the main challenges is the development of drug resistance, which limits the long-term efficacy of PDGFR inhibitors. Secondary mutations in PDGFR, activation of alternative signaling pathways, and tumor microenvironment changes are among the main mechanisms of resistance. Another challenge is the off-target effects of multi-targeted PDGFR inhibitors, which can lead to adverse events such as hypertension, fatigue, and gastrointestinal toxicity. Future research directions include the development of more selective PDGFR inhibitors that target specific PDGFR isoforms or mutations, the identification of novel biomarkers for predicting response to PDGFR inhibitors, and the combination of PDGFR inhibitors with other therapeutic agents (such as immunotherapies) to overcome resistance and improve efficacy. In addition, further studies are needed to understand the role of PDGFR signaling in the tumor microenvironment and its interaction with immune cells, which may provide new opportunities for the development of combination therapies.
In conclusion, PDGFR inhibitors have become an important class of targeted therapeutic agents in cancer treatment, with significant progress made in understanding their mechanism of action, developing novel inhibitors, and optimizing their clinical application. The identification of PDGFR mutations and the characterization of PDGFR signaling pathways have provided critical insights into the molecular basis of cancer, guiding the development of personalized therapeutic strategies. Despite the challenges, ongoing research in PDGFR inhibitors holds great promise for improving the prognosis of cancer patients with dysregulated PDGFR signaling.