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

Primary targets: C_MET · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
99.75
Gini
0.582
CATDS
0.046

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 Capmatinib. Strongest target: C_MET at 99.5% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1C_MET99.5%0.5%
2EGFR63.1%36.9%
3ROS_ROS160.2%39.8%
4JAK353.5%46.5%
5RON_MST1R26.4%73.6%
6MST3_STK2422.2%77.8%
7SRPK220.8%79.2%
8HASPIN20.7%79.3%
9AXL20.1%79.9%
10MYLK419.7%80.3%
11RIPK219.3%80.7%
12PDGFRB17.9%82.1%
13ERBB4_HER417.3%82.7%
14EIF2AK217.0%83.0%
15STK32B_YANK216.4%83.6%
16ABL2_ARG15.9%84.1%
17CAMKK215.8%84.2%
18PKN3_PRK315.7%84.3%
19PDK3_PDHK315.4%84.6%
20CAMK1D15.1%84.9%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Capmatinib

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
697.17
ALLOGRAFT_REJECTION
1539.33
ANDROGEN_RESPONSE
859.75
ANGIOGENESIS
352.81
APICAL_JUNCTION
2059.82
APICAL_SURFACE
251.42
APOPTOSIS
1967.95
BILE_ACID_METABOLISM
261.27
CHOLESTEROL_HOMEOSTASIS
499.25
COAGULATION
192.92
COMPLEMENT
1373.27
DNA_REPAIR
596.08
E2F_TARGETS
1820.06
EPITHELIAL_MESENCHYMAL_TRANSITION
660.67
ESTROGEN_RESPONSE_EARLY
1100.81
ESTROGEN_RESPONSE_LATE
996.44
FATTY_ACID_METABOLISM
135.79
G2M_CHECKPOINT
1580.01
GLYCOLYSIS
715.13
HEDGEHOG_SIGNALING
288.61
HEME_METABOLISM
510.03
HYPOXIA
1202.85
IL2_STAT5_SIGNALING
762.96
IL6_JAK_STAT3_SIGNALING
1088.99
INFLAMMATORY_RESPONSE
1305.48
INTERFERON_ALPHA_RESPONSE
243.56
INTERFERON_GAMMA_RESPONSE
1539.52
KRAS_SIGNALING_DN
389.03
KRAS_SIGNALING_UP
729.69
MITOTIC_SPINDLE
1631.74
MTORC1_SIGNALING
1023.05
MYC_TARGETS_V1
1079.09
MYC_TARGETS_V2
262.16
MYOGENESIS
975.22
NOTCH_SIGNALING
139.24
OXIDATIVE_PHOSPHORYLATION
313.89
P53_PATHWAY
1080.53
PANCREAS_BETA_CELLS
140.52
PEROXISOME
322.06
PI3K_AKT_MTOR_SIGNALING
2052.36
PROTEIN_SECRETION
612.42
REACTIVE_OXYGEN_SPECIES_PATHWAY
154.43
SPERMATOGENESIS
486.58
TGF_BETA_SIGNALING
623.38
TNFA_SIGNALING_VIA_NFKB
1503.62
UNFOLDED_PROTEIN_RESPONSE
496.06
UV_RESPONSE_DN
1175.44
UV_RESPONSE_UP
1004.75
WNT_BETA_CATENIN_SIGNALING
740.22
XENOBIOTIC_METABOLISM
501.92

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 = 3.13 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 = 0.883

SampleCancer typecos to ideal
EPT0291EPN0.883
TCGA-CF-A5U8-01A-11R-A28M-070.863
SRR122024980.852
SRR233037520.852
aMVAC.P_005_TURBT_S2230.852

Annotations

Sign in to read and post annotations.

Loading…