TAS-120 (Futibatinib, TAS120) is a highly potent, selective, irreversible pan-FGFR inhibitor with IC50 of 0.9 nM for wt FGFR2; inhibits cancer cell growth in vitro and shows promising activity in human xenografts of FGFR mutation-bearing tumours; TAS-120 inhibits mutant and wild-type FGFR2 with similar IC50 (wild-type FGFR2, 0.9 nM; V565I 1.3 nM; N550H, 3.6 nM; E566G, 2.4 nM) and has shown efficacy in FGFR inhibitor-resistant cell lines.

A novel aniline compound that mimics the neuroprotective effects of bFGF by activating FGFR1-MEK/ERK signaling pathway; prevents glutamate-induced neuronal death in primary cultures of rat cerebrocortical neurons, augments phosphorylation of FGFR-1 and ERK-1/2, increases the levels of CALB1 gene expression; increases the levels of newly synthesized calcium-binding protein calbindin-D28k (Calb) in cerebrocortical neurons and suppresses the glutamate-induced rise in intracellular Ca(2+) in WT mice; attenuates neuronal damage and cognitive deficits in a rat model of Alzheimer's disease.

A selective FGFR1 inhibitor with IC50 of 10-20 uM; does not inhibit tyrosine phosphorylation of PDGFR and EGFR (IC50>200 uM), weakly inhibits insulin receptor; specifically inhibits the growth of the t(4;14)-positive MM lines, KMS-11 and OPM-2, reduces cell viability and increases apoptosis.

Rogaratinib (BAY 1163877) is a potent, selective, orally available pan-FGFR with IC50 of 15, <1, 19 and 33 nM for FGFR1, 2, 3 and 4, respectively; weakly inhibits VEGFR2 with IC50 of 120 nM, exhibits Ki of 1.6, 5.0, 7.8 and 7.6 nM for FGFR1, 2, 3 and 4 in competition binding assay, no significant affitnity for VEGFR2 (19% inhibition at 100 nM); inhibits FGFb-stimulated HUVEC proliferation with IC50 of 16 nM, 28-fold selectivity over VEGF-stimulated; demonstrates tumor growth reduction in pre-clinical models bearing different FGFR alterations both in mono- and combination therapy.

PRN-1371 (PRN1371)?is a potent, selective, irreversible covalent, orally active pan-FGFR inhibitor with IC50 of 0.6/1.3/4.1/19.3 nM for FGFR1/2/3/4, respectively; demonstrates excellent kinome-wide selectivity in a number of biochemical and cellular assays; exhibits sustained inhibition of FGFR in multiple tumor xenografts and patient-derived tumor xenograft models.

A potent, selective, ATP-competitive FGFR1 inhibitor with IC50 of ~25 nM; also inhibits autophosphorylation of VEGFR2 with IC50 of 100–200 nM; displays >1000-fold selectivity over Src, InsR, EGFR, PDGFR, etc.

PD-166866 is a potent, selective, ATP competitive FGFR-1 inhibitor with IC50 of 52.4 nM, has no effect on c-Src, PDGFR-β, EGFR or InsR tyrosine kinases or on MEK, PKC and CDK4 (IC50>50 uM); inhibits FGFR-1 autophosphorylation in NIH 3T3 cells and L6 cells with IC50 of 10.8 and 3.1 nM, respectively; inhibits bFGF-stimulated cell growth of L6 cells with IC50 of 24.1 nM, also is a a potent inhibitor of microvessel outgrowth (angiogenesis) from cultured artery fragments of human placenta.

ODM-203 (ODM203) is a potent, selective, dual inhibitor of FGFR and VEGFR tyrosine kinases with approximately equal potency towards recombinant FGFR1, 2, 3 and 4, as well as VEGFR1, 2 and 3 (IC50=5-35 nM); suppresses 9/317 additional kinases by >70% at 1 uM, 9 kinases suppressed by ODM-203 - DDR1, MAP4K4, MINK1, RET, PDGFRa and SIK2 (IC50<100 nM); ODM-203 is a potent inhibitor of FGFR signaling and proliferation in several FGFR-dependent cell lines; ODM-203 inhibits VEGFR-induced tube formation (IC50 33 nM) with similar potency as it inhibits proliferation in FGFR-dependent cell lines (IC50 50-150 nM); inhibits FGFR phosphorylation and tumor growth in several FGFR-dependent xenografts.

NVP-BGJ398 phosphate (Infigratinib phosphate, BGJ398 phosphate) is a potent, selective pan-FGFR inhibitor with IC50 of 0.9/1.0/1.4/60 nM for FGFR1/2/3/4, also shows high potenct against mutant FGFR3-K650E with IC50 of 4.9 nM; inhibits the proliferation of the FGFR1-, FGFR2-, and FGFR3-dependent BaF3 cells with IC50 of low nanomolar range; shows significant antitumor activity in RT112 bladder cancer xenografts models overexpressing wild-type FGFR3, significantly inhibits the growth of FGFR2-mutated endometrial cancer xenograft models, also ameliorates FGF23-mediated hypophosphatemic rickets in mouse models.

An orally active small-molecule chemical that acts as an extracellular FGF trap, binds immobilized FGF3,FGF4, FGF6, FGF8, FGF16, FGF18, FGF20, and FGF22 with Kd of 16-120 uM, inhibits FGF-dependent tumor growth, angiogenesis and metastases; shows no apparent interaction for the other FGFs; inhibits HSPG/FGF/FGFR ternary complex formation induced by FGFR1(IIIc)-binding FGFs KATO III cells, inhibits FGFR1 phosphorylation in HUVECs stimulated by FGF2 with inhibition of HUVEC proliferation with IC50 of 6.5 uM; demonstrates significant inhibition of H520 tumor growth in vivo.