Research Use Only. KIRhub outputs are computational research artifacts. They are not validated for clinical decision-making, diagnosis, or treatment.

Primary targets: FGFR2 · FDA status: FDA Approval Withdrawn

Selectivity scorecard

MeasuredDerived
KISS
98.24
Gini
0.710
CATDS
0.025

Computed from wild-type kinome inhibition at 1 μM. Gini reproduces the published values within tolerance; KISS and CATDS are computed but pending reconciliation with the paper's reference code.

Polypharmacology radar

MeasuredDerived

Top 20 strongest-inhibited wild-type kinases for Infigratinib. Strongest target: FGFR1 at 99.2% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1FGFR199.2%0.8%
2FGFR298.8%1.2%
3FMS98.7%1.3%
4FGFR398.6%1.4%
5FGFR494.7%5.3%
6TAOK2_TAO193.3%6.7%
7DDR191.7%8.3%
8LCK88.0%12.0%
9LYN79.6%20.4%
10C_KIT71.8%28.2%
11FLT4_VEGFR369.4%30.6%
12TIE2_TEK68.9%31.1%
13FLT1_VEGFR167.5%32.5%
14MEKK362.5%37.5%
15EIF2AK261.7%38.3%
16CDK4_CYCLIN_D359.4%40.6%
17YES_YES156.7%43.3%
18TAOK154.7%45.3%
19EIF2AK452.6%47.4%
20NEK251.0%49.0%

Selectivity landscape

MeasuredDerived

Where Infigratinib sits in the 92-drug selectivity landscape (KISS vs Gini). The highlighted point is Infigratinib.

Atlas insights for Infigratinib

MeasuredReference

Pathway-space view of what this drug actually does, drawn from the Pathway Atlas.

On-target vs off-target shadow

DerivedMeasured

How much of this drug's pathway perturbation comes from primary targets vs polypharmacology vs 2nd-order propagation. When off-target dominates, the FDA label is the smallest description of the drug.

On-target3%
Off-target97%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
1183.73
ALLOGRAFT_REJECTION
4830.52
ANDROGEN_RESPONSE
889.23
ANGIOGENESIS
730.02
APICAL_JUNCTION
5043.30
APICAL_SURFACE
390.08
APOPTOSIS
3142.33
BILE_ACID_METABOLISM
379.65
CHOLESTEROL_HOMEOSTASIS
516.35
COAGULATION
532.18
COMPLEMENT
2490.16
DNA_REPAIR
915.50
E2F_TARGETS
2255.98
EPITHELIAL_MESENCHYMAL_TRANSITION
916.44
ESTROGEN_RESPONSE_EARLY
1418.83
ESTROGEN_RESPONSE_LATE
1584.20
FATTY_ACID_METABOLISM
496.70
G2M_CHECKPOINT
2114.69
GLYCOLYSIS
1650.67
HEDGEHOG_SIGNALING
335.71
HEME_METABOLISM
1194.31
HYPOXIA
1766.91
IL2_STAT5_SIGNALING
1435.12
IL6_JAK_STAT3_SIGNALING
2865.72
INFLAMMATORY_RESPONSE
2164.60
INTERFERON_ALPHA_RESPONSE
383.44
INTERFERON_GAMMA_RESPONSE
3200.03
KRAS_SIGNALING_DN
426.98
KRAS_SIGNALING_UP
1921.10
MITOTIC_SPINDLE
3211.33
MTORC1_SIGNALING
2161.67
MYC_TARGETS_V1
2035.49
MYC_TARGETS_V2
425.73
MYOGENESIS
1299.70
NOTCH_SIGNALING
63.95
OXIDATIVE_PHOSPHORYLATION
1032.81
P53_PATHWAY
1691.73
PANCREAS_BETA_CELLS
167.32
PEROXISOME
555.57
PI3K_AKT_MTOR_SIGNALING
5151.20
PROTEIN_SECRETION
1034.07
REACTIVE_OXYGEN_SPECIES_PATHWAY
248.04
SPERMATOGENESIS
754.67
TGF_BETA_SIGNALING
791.44
TNFA_SIGNALING_VIA_NFKB
1782.63
UNFOLDED_PROTEIN_RESPONSE
790.02
UV_RESPONSE_DN
2383.93
UV_RESPONSE_UP
1798.14
WNT_BETA_CATENIN_SIGNALING
922.68
XENOBIOTIC_METABOLISM
1086.03

See this drug on the perturbation map →

Hallmarks-of-Cancer reach

DerivedReference

Projection onto the 10 canonical Hanahan & Weinberg hallmarks. Breadth = how many hallmarks this drug meaningfully perturbs.

ProliferationEvading apoptosisAngiogenesisInvasion / metastasisReplicative immortalityDeregulated metabolismImmune evasionGenome instabilityInflammationGrowth signaling

Breadth = 3.10 bits (max possible across 10 hallmarks = 3.32 bits). Multi-hallmark agent — broad polypharmacology.

Compare against the full catalog →

Anti-tumor matches — the "ideal patient" search

ModeledDerived

Top 5 real tumors closest to this drug's ideal patient (the tumor whose pathway state = −Π_d). Closest match cosine = 0.822

SampleCancer typecos to ideal
EPT0291EPN0.822
SRR233037520.820
aMVAC.P_005_TURBT_S2230.804
C3N-034200.803
TCGA-CF-A5U8-01A-11R-A28M-070.803

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