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
0.689
CATDS
0.063

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 Binimetinib. Strongest target: MEK1 at 79.1% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1MEK179.1%20.9%
2MEK243.5%56.5%
3CDK9_CYCLIN_T133.3%66.7%
4CAMKK223.0%77.0%
5EGFR21.8%78.3%
6ALK3_BMPR1A20.2%79.8%
7TTBK220.0%80.0%
8TGFBR219.7%80.3%
9PDK2_PDHK216.9%83.1%
10MUSK15.4%84.6%
11CAMK2A15.4%84.6%
12LYN15.4%84.6%
13HASPIN14.4%85.6%
14HIPK113.9%86.1%
15VRK213.3%86.7%
16VRK112.5%87.5%
17P38A_MAPK1412.3%87.7%
18STK21_CIT12.2%87.8%
19BRAF12.2%87.8%
20PHKG111.5%88.5%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Binimetinib

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
267.22
ALLOGRAFT_REJECTION
730.96
ANDROGEN_RESPONSE
317.92
ANGIOGENESIS
128.79
APICAL_JUNCTION
871.94
APICAL_SURFACE
84.38
APOPTOSIS
922.88
BILE_ACID_METABOLISM
153.42
CHOLESTEROL_HOMEOSTASIS
197.42
COAGULATION
59.14
COMPLEMENT
584.80
DNA_REPAIR
233.89
E2F_TARGETS
831.40
EPITHELIAL_MESENCHYMAL_TRANSITION
330.21
ESTROGEN_RESPONSE_EARLY
470.61
ESTROGEN_RESPONSE_LATE
411.34
FATTY_ACID_METABOLISM
58.41
G2M_CHECKPOINT
590.79
GLYCOLYSIS
412.65
HEDGEHOG_SIGNALING
100.65
HEME_METABOLISM
204.13
HYPOXIA
541.35
IL2_STAT5_SIGNALING
290.84
IL6_JAK_STAT3_SIGNALING
436.50
INFLAMMATORY_RESPONSE
547.52
INTERFERON_ALPHA_RESPONSE
95.12
INTERFERON_GAMMA_RESPONSE
591.78
KRAS_SIGNALING_DN
183.00
KRAS_SIGNALING_UP
387.09
MITOTIC_SPINDLE
662.66
MTORC1_SIGNALING
453.66
MYC_TARGETS_V1
495.40
MYC_TARGETS_V2
117.29
MYOGENESIS
456.81
NOTCH_SIGNALING
89.72
OXIDATIVE_PHOSPHORYLATION
81.29
P53_PATHWAY
427.23
PANCREAS_BETA_CELLS
43.15
PEROXISOME
126.37
PI3K_AKT_MTOR_SIGNALING
994.61
PROTEIN_SECRETION
263.19
REACTIVE_OXYGEN_SPECIES_PATHWAY
39.64
SPERMATOGENESIS
291.77
TGF_BETA_SIGNALING
303.19
TNFA_SIGNALING_VIA_NFKB
511.15
UNFOLDED_PROTEIN_RESPONSE
184.41
UV_RESPONSE_DN
513.00
UV_RESPONSE_UP
525.85
WNT_BETA_CATENIN_SIGNALING
436.15
XENOBIOTIC_METABOLISM
202.14

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 = 3.15 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 = 0.869

SampleCancer typecos to ideal
EPT0291EPN0.869
TCGA-CF-A5U8-01A-11R-A28M-070.851
SRR233037520.838
aMVAC.P_005_TURBT_S2230.833
SRR122024980.831

Annotations

Sign in to read and post annotations.

Loading…