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

Primary targets: FGFR1, FGFR2, FGFR3 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
90.23
Gini
0.608
CATDS
0.008

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 Nintedanib. Strongest target: DDR2 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1DDR2100.0%0.0%
2LCK100.0%0.0%
3RET100.0%0.0%
4ABL199.9%0.1%
5MELK99.4%0.6%
6SIK299.4%0.6%
7FLT4_VEGFR399.2%0.8%
8MEK598.6%1.4%
9PDGFRA98.3%1.7%
10BTK98.0%2.0%
11LYN97.9%2.1%
12YES_YES197.9%2.1%
13BLK97.6%2.4%
14FGFR297.0%3.0%
15C_SRC96.9%3.1%
16C_KIT96.8%3.2%
17TRKC96.7%3.3%
18KDR_VEGFR296.4%3.6%
19DDR196.1%3.9%
20PDGFRB96.0%4.0%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Nintedanib

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-target0%
Off-target100%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
3751.59
ALLOGRAFT_REJECTION
12688.86
ANDROGEN_RESPONSE
2757.09
ANGIOGENESIS
2235.01
APICAL_JUNCTION
12843.57
APICAL_SURFACE
1352.03
APOPTOSIS
10479.60
BILE_ACID_METABOLISM
1327.74
CHOLESTEROL_HOMEOSTASIS
1822.59
COAGULATION
1467.82
COMPLEMENT
7199.69
DNA_REPAIR
2602.05
E2F_TARGETS
5936.72
EPITHELIAL_MESENCHYMAL_TRANSITION
2916.27
ESTROGEN_RESPONSE_EARLY
4588.92
ESTROGEN_RESPONSE_LATE
4379.27
FATTY_ACID_METABOLISM
1192.04
G2M_CHECKPOINT
6679.60
GLYCOLYSIS
4059.89
HEDGEHOG_SIGNALING
1508.79
HEME_METABOLISM
2725.70
HYPOXIA
5720.51
IL2_STAT5_SIGNALING
4297.93
IL6_JAK_STAT3_SIGNALING
7358.40
INFLAMMATORY_RESPONSE
6691.19
INTERFERON_ALPHA_RESPONSE
1186.47
INTERFERON_GAMMA_RESPONSE
8715.59
KRAS_SIGNALING_DN
1572.48
KRAS_SIGNALING_UP
4615.23
MITOTIC_SPINDLE
8917.87
MTORC1_SIGNALING
5286.50
MYC_TARGETS_V1
4102.45
MYC_TARGETS_V2
1045.14
MYOGENESIS
4694.25
NOTCH_SIGNALING
332.43
OXIDATIVE_PHOSPHORYLATION
1860.68
P53_PATHWAY
5278.86
PANCREAS_BETA_CELLS
372.99
PEROXISOME
1822.99
PI3K_AKT_MTOR_SIGNALING
12684.96
PROTEIN_SECRETION
2811.76
REACTIVE_OXYGEN_SPECIES_PATHWAY
806.26
SPERMATOGENESIS
2042.04
TGF_BETA_SIGNALING
3178.25
TNFA_SIGNALING_VIA_NFKB
6466.05
UNFOLDED_PROTEIN_RESPONSE
1986.02
UV_RESPONSE_DN
7246.75
UV_RESPONSE_UP
4968.36
WNT_BETA_CATENIN_SIGNALING
2891.62
XENOBIOTIC_METABOLISM
3000.29

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 = 3.11 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 = 0.839

SampleCancer typecos to ideal
EPT0291EPN0.839
SRR233037520.836
SRR108999840.825
aMVAC.P_005_TURBT_S2230.823
TCGA-CF-A5U8-01A-11R-A28M-070.821

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