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

Primary targets: MEK1, MEK2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
100.00
Gini
0.644
CATDS
0.048

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 Cobimetinib. Strongest target: MEK1 at 73.5% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1MEK173.5%26.4%
2MEK259.8%40.2%
3TNIK30.5%69.5%
4MINK_MINK121.7%78.3%
5ERN1_IRE121.3%78.7%
6ALK2_ACVR121.3%78.7%
7C_MET18.7%81.3%
8MST3_STK2418.3%81.7%
9GRK618.1%81.9%
10AURORA_B17.2%82.8%
11STK32C_YANK316.5%83.5%
12FLT316.0%84.0%
13TRPM7_CHAK115.1%84.9%
14ALK6_BMPR1B14.7%85.3%
15CK1G213.9%86.1%
16COT1_MAP3K813.4%86.6%
17TLK112.6%87.4%
18CK2A212.5%87.5%
19MLK412.0%88.0%
20ERK112.0%88.0%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Cobimetinib

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
267.74
ALLOGRAFT_REJECTION
773.52
ANDROGEN_RESPONSE
216.86
ANGIOGENESIS
124.22
APICAL_JUNCTION
853.10
APICAL_SURFACE
118.05
APOPTOSIS
897.25
BILE_ACID_METABOLISM
137.13
CHOLESTEROL_HOMEOSTASIS
185.18
COAGULATION
95.91
COMPLEMENT
561.56
DNA_REPAIR
282.13
E2F_TARGETS
761.82
EPITHELIAL_MESENCHYMAL_TRANSITION
212.54
ESTROGEN_RESPONSE_EARLY
438.68
ESTROGEN_RESPONSE_LATE
368.41
FATTY_ACID_METABOLISM
104.56
G2M_CHECKPOINT
692.10
GLYCOLYSIS
318.75
HEDGEHOG_SIGNALING
105.29
HEME_METABOLISM
263.26
HYPOXIA
552.81
IL2_STAT5_SIGNALING
375.17
IL6_JAK_STAT3_SIGNALING
502.94
INFLAMMATORY_RESPONSE
567.09
INTERFERON_ALPHA_RESPONSE
91.94
INTERFERON_GAMMA_RESPONSE
587.88
KRAS_SIGNALING_DN
140.28
KRAS_SIGNALING_UP
374.62
MITOTIC_SPINDLE
827.97
MTORC1_SIGNALING
430.18
MYC_TARGETS_V1
467.75
MYC_TARGETS_V2
113.18
MYOGENESIS
438.73
NOTCH_SIGNALING
92.55
OXIDATIVE_PHOSPHORYLATION
175.76
P53_PATHWAY
489.28
PANCREAS_BETA_CELLS
36.20
PEROXISOME
151.00
PI3K_AKT_MTOR_SIGNALING
950.22
PROTEIN_SECRETION
194.38
REACTIVE_OXYGEN_SPECIES_PATHWAY
69.65
SPERMATOGENESIS
212.91
TGF_BETA_SIGNALING
288.32
TNFA_SIGNALING_VIA_NFKB
560.38
UNFOLDED_PROTEIN_RESPONSE
219.59
UV_RESPONSE_DN
528.04
UV_RESPONSE_UP
456.36
WNT_BETA_CATENIN_SIGNALING
375.36
XENOBIOTIC_METABOLISM
213.44

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 = 0.873

SampleCancer typecos to ideal
EPT0291EPN0.873
TCGA-CF-A5U8-01A-11R-A28M-070.852
SRR233037520.844
SRR122024980.843
SRR1443713GTEX0.841

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