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

Primary targets: BRAF · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
96.49
Gini
0.598
CATDS
0.011

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 Vemurafenib. Strongest target: LCK at 98.4% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1LCK98.4%1.6%
2KHS_MAP4K598.3%1.7%
3MEK298.1%1.9%
4BRK98.0%2.0%
5ARAF96.9%3.1%
6MYLK495.8%4.2%
7SRMS95.3%4.7%
8RAF195.2%4.8%
9RIPK394.5%5.5%
10MEK594.4%5.6%
11TNIK94.4%5.6%
12FGR93.6%6.4%
13ZAK_MLTK92.9%7.1%
14BRAF92.8%7.2%
15MLCK2_MYLK289.6%10.4%
16DDR289.4%10.6%
17MST1_STK489.0%11.0%
18WNK388.5%11.5%
19BLK87.8%12.2%
20TGFBR286.4%13.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Vemurafenib

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-target1%
Off-target99%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
3113.85
ALLOGRAFT_REJECTION
8338.88
ANDROGEN_RESPONSE
1976.28
ANGIOGENESIS
1431.24
APICAL_JUNCTION
8717.77
APICAL_SURFACE
951.15
APOPTOSIS
7588.57
BILE_ACID_METABOLISM
707.78
CHOLESTEROL_HOMEOSTASIS
1162.81
COAGULATION
1122.48
COMPLEMENT
4945.72
DNA_REPAIR
2004.79
E2F_TARGETS
5691.73
EPITHELIAL_MESENCHYMAL_TRANSITION
2238.19
ESTROGEN_RESPONSE_EARLY
3716.92
ESTROGEN_RESPONSE_LATE
3266.41
FATTY_ACID_METABOLISM
783.58
G2M_CHECKPOINT
6224.94
GLYCOLYSIS
2449.82
HEDGEHOG_SIGNALING
786.57
HEME_METABOLISM
2452.01
HYPOXIA
4348.70
IL2_STAT5_SIGNALING
3917.71
IL6_JAK_STAT3_SIGNALING
5211.98
INFLAMMATORY_RESPONSE
5385.20
INTERFERON_ALPHA_RESPONSE
1231.05
INTERFERON_GAMMA_RESPONSE
6339.84
KRAS_SIGNALING_DN
1049.29
KRAS_SIGNALING_UP
3394.23
MITOTIC_SPINDLE
6662.35
MTORC1_SIGNALING
4102.43
MYC_TARGETS_V1
4540.95
MYC_TARGETS_V2
1096.49
MYOGENESIS
3187.01
NOTCH_SIGNALING
358.58
OXIDATIVE_PHOSPHORYLATION
1311.23
P53_PATHWAY
4405.97
PANCREAS_BETA_CELLS
525.53
PEROXISOME
1113.07
PI3K_AKT_MTOR_SIGNALING
9004.25
PROTEIN_SECRETION
1997.90
REACTIVE_OXYGEN_SPECIES_PATHWAY
690.00
SPERMATOGENESIS
1820.88
TGF_BETA_SIGNALING
2333.54
TNFA_SIGNALING_VIA_NFKB
5389.60
UNFOLDED_PROTEIN_RESPONSE
1582.89
UV_RESPONSE_DN
5469.34
UV_RESPONSE_UP
3797.54
WNT_BETA_CATENIN_SIGNALING
2149.82
XENOBIOTIC_METABOLISM
1677.57

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 = 3.09 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 = 0.863

SampleCancer typecos to ideal
EPT0291EPN0.863
TCGA-CF-A5U8-01A-11R-A28M-070.847
SRR233037520.846
SRR122024980.842
aMVAC.P_005_TURBT_S2230.840

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