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 Approved

Selectivity scorecard

MeasuredDerived
KISS
98.23
Gini
0.718
CATDS
0.022

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 Pemigatinib. Strongest target: FGFR1 at 99.9% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1FGFR199.9%0.1%
2FGFR399.4%0.6%
3FGFR298.7%1.3%
4EIF2AK197.7%2.3%
5FMS95.5%4.5%
6FGFR493.9%6.1%
7FLT4_VEGFR392.1%7.9%
8EIF2AK285.3%14.7%
9FLT1_VEGFR184.7%15.3%
10MLK2_MAP3K1081.3%18.7%
11TAOK2_TAO180.3%19.7%
12SIK379.4%20.6%
13MST3_STK2474.4%25.6%
14STK25_YSK172.5%27.5%
15GLK_MAP4K370.8%29.2%
16MEKK267.2%32.8%
17C_KIT65.4%34.6%
18CDK6_CYCLIN_D363.3%36.7%
19LYN61.7%38.3%
20NEK159.0%41.0%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Pemigatinib

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
1200.51
ALLOGRAFT_REJECTION
4014.42
ANDROGEN_RESPONSE
1111.07
ANGIOGENESIS
655.23
APICAL_JUNCTION
4331.61
APICAL_SURFACE
380.90
APOPTOSIS
2972.47
BILE_ACID_METABOLISM
521.28
CHOLESTEROL_HOMEOSTASIS
662.12
COAGULATION
417.68
COMPLEMENT
2533.10
DNA_REPAIR
996.31
E2F_TARGETS
2472.48
EPITHELIAL_MESENCHYMAL_TRANSITION
807.65
ESTROGEN_RESPONSE_EARLY
1475.64
ESTROGEN_RESPONSE_LATE
1536.52
FATTY_ACID_METABOLISM
575.53
G2M_CHECKPOINT
1944.34
GLYCOLYSIS
1618.59
HEDGEHOG_SIGNALING
287.91
HEME_METABOLISM
992.37
HYPOXIA
2171.16
IL2_STAT5_SIGNALING
1384.49
IL6_JAK_STAT3_SIGNALING
2902.27
INFLAMMATORY_RESPONSE
2066.98
INTERFERON_ALPHA_RESPONSE
305.66
INTERFERON_GAMMA_RESPONSE
3237.39
KRAS_SIGNALING_DN
428.54
KRAS_SIGNALING_UP
1678.47
MITOTIC_SPINDLE
2793.59
MTORC1_SIGNALING
1944.10
MYC_TARGETS_V1
1582.28
MYC_TARGETS_V2
305.31
MYOGENESIS
1418.35
NOTCH_SIGNALING
141.90
OXIDATIVE_PHOSPHORYLATION
937.26
P53_PATHWAY
1623.21
PANCREAS_BETA_CELLS
252.64
PEROXISOME
420.97
PI3K_AKT_MTOR_SIGNALING
5094.29
PROTEIN_SECRETION
1097.21
REACTIVE_OXYGEN_SPECIES_PATHWAY
177.75
SPERMATOGENESIS
620.09
TGF_BETA_SIGNALING
885.96
TNFA_SIGNALING_VIA_NFKB
1873.26
UNFOLDED_PROTEIN_RESPONSE
734.30
UV_RESPONSE_DN
2150.27
UV_RESPONSE_UP
1761.36
WNT_BETA_CATENIN_SIGNALING
972.18
XENOBIOTIC_METABOLISM
1052.17

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 = 3.12 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 = 0.840

SampleCancer typecos to ideal
EPT0291EPN0.840
SRR233037520.831
SRR108999840.816
aMVAC.P_005_TURBT_S2230.816
TCGA-CF-A5U8-01A-11R-A28M-070.814

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