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

Primary targets: FGFR1 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
95.71
Gini
0.737
CATDS
0.018

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 Erdafitinib. Strongest target: FGFR3 at 99.1% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1FGFR399.1%0.9%
2FGFR299.0%1.0%
3FGFR199.0%1.0%
4FGFR498.0%2.0%
5C_KIT98.0%2.0%
6FLT4_VEGFR397.9%2.1%
7LYN97.8%2.2%
8FMS97.6%2.4%
9EIF2AK297.0%3.0%
10FLT1_VEGFR196.6%3.4%
11DDR195.8%4.2%
12RET94.7%5.3%
13PDGFRA94.5%5.5%
14DDR293.5%6.5%
15KDR_VEGFR291.8%8.2%
16LCK91.7%8.3%
17ABL190.9%9.1%
18EPHB489.7%10.3%
19EPHB189.3%10.7%
20EPHA587.6%12.4%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Erdafitinib

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-target4%
Off-target96%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
2081.12
ALLOGRAFT_REJECTION
7870.08
ANDROGEN_RESPONSE
1104.34
ANGIOGENESIS
1500.73
APICAL_JUNCTION
8629.03
APICAL_SURFACE
755.47
APOPTOSIS
5552.60
BILE_ACID_METABOLISM
664.98
CHOLESTEROL_HOMEOSTASIS
1219.37
COAGULATION
1086.87
COMPLEMENT
4832.35
DNA_REPAIR
1467.72
E2F_TARGETS
3246.83
EPITHELIAL_MESENCHYMAL_TRANSITION
1445.04
ESTROGEN_RESPONSE_EARLY
2435.78
ESTROGEN_RESPONSE_LATE
2227.32
FATTY_ACID_METABOLISM
757.39
G2M_CHECKPOINT
3605.79
GLYCOLYSIS
2313.95
HEDGEHOG_SIGNALING
760.93
HEME_METABOLISM
1756.20
HYPOXIA
3401.20
IL2_STAT5_SIGNALING
2666.27
IL6_JAK_STAT3_SIGNALING
4432.77
INFLAMMATORY_RESPONSE
3739.22
INTERFERON_ALPHA_RESPONSE
714.71
INTERFERON_GAMMA_RESPONSE
5182.49
KRAS_SIGNALING_DN
684.21
KRAS_SIGNALING_UP
3098.51
MITOTIC_SPINDLE
5691.66
MTORC1_SIGNALING
3045.07
MYC_TARGETS_V1
2793.81
MYC_TARGETS_V2
636.40
MYOGENESIS
2124.01
NOTCH_SIGNALING
148.51
OXIDATIVE_PHOSPHORYLATION
1325.75
P53_PATHWAY
3005.31
PANCREAS_BETA_CELLS
315.65
PEROXISOME
858.26
PI3K_AKT_MTOR_SIGNALING
8096.49
PROTEIN_SECRETION
1700.36
REACTIVE_OXYGEN_SPECIES_PATHWAY
464.38
SPERMATOGENESIS
1048.79
TGF_BETA_SIGNALING
1567.18
TNFA_SIGNALING_VIA_NFKB
2943.40
UNFOLDED_PROTEIN_RESPONSE
970.38
UV_RESPONSE_DN
4245.22
UV_RESPONSE_UP
2923.70
WNT_BETA_CATENIN_SIGNALING
1382.80
XENOBIOTIC_METABOLISM
1633.89

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 = 0.820

SampleCancer typecos to ideal
SRR233037520.820
EPT0291EPN0.818
aMVAC.P_005_TURBT_S2230.805
SRR108999840.803
TCGA-CF-A5U8-01A-11R-A28M-070.801

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