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
98.50
Gini
0.755
CATDS
0.029

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 Encorafenib. Strongest target: RAF1 at 99.7% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1RAF199.7%0.3%
2BRAF98.0%2.0%
3IRAK197.5%2.5%
4ARAF97.4%2.6%
5LIMK293.9%6.1%
6GSK3B91.5%8.5%
7LIMK188.5%11.5%
8JNK382.1%17.9%
9RIPK376.6%23.4%
10NLK71.3%28.6%
11JNK169.9%30.1%
12JNK265.6%34.4%
13ZAK_MLTK63.5%36.5%
14MLK2_MAP3K1062.1%37.9%
15HIPK454.2%45.8%
16P38A_MAPK1453.5%46.5%
17CK1G252.6%47.4%
18TESK252.3%47.7%
19PDK2_PDHK248.5%51.5%
20MKK648.4%51.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Encorafenib

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-target2%
Off-target98%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
1885.33
ALLOGRAFT_REJECTION
2366.36
ANDROGEN_RESPONSE
1600.58
ANGIOGENESIS
323.46
APICAL_JUNCTION
2416.73
APICAL_SURFACE
351.99
APOPTOSIS
4542.50
BILE_ACID_METABOLISM
420.57
CHOLESTEROL_HOMEOSTASIS
375.33
COAGULATION
338.04
COMPLEMENT
1886.78
DNA_REPAIR
1555.13
E2F_TARGETS
4580.13
EPITHELIAL_MESENCHYMAL_TRANSITION
1543.90
ESTROGEN_RESPONSE_EARLY
2358.24
ESTROGEN_RESPONSE_LATE
2208.10
FATTY_ACID_METABOLISM
375.89
G2M_CHECKPOINT
4913.97
GLYCOLYSIS
1191.65
HEDGEHOG_SIGNALING
402.30
HEME_METABOLISM
1712.27
HYPOXIA
2525.57
IL2_STAT5_SIGNALING
2151.15
IL6_JAK_STAT3_SIGNALING
1469.37
INFLAMMATORY_RESPONSE
2471.10
INTERFERON_ALPHA_RESPONSE
528.23
INTERFERON_GAMMA_RESPONSE
2723.74
KRAS_SIGNALING_DN
785.53
KRAS_SIGNALING_UP
1163.58
MITOTIC_SPINDLE
3079.16
MTORC1_SIGNALING
1982.55
MYC_TARGETS_V1
2824.49
MYC_TARGETS_V2
698.95
MYOGENESIS
2199.02
NOTCH_SIGNALING
380.87
OXIDATIVE_PHOSPHORYLATION
384.72
P53_PATHWAY
2895.45
PANCREAS_BETA_CELLS
518.88
PEROXISOME
739.40
PI3K_AKT_MTOR_SIGNALING
4393.26
PROTEIN_SECRETION
889.46
REACTIVE_OXYGEN_SPECIES_PATHWAY
398.64
SPERMATOGENESIS
1211.05
TGF_BETA_SIGNALING
1697.35
TNFA_SIGNALING_VIA_NFKB
3950.03
UNFOLDED_PROTEIN_RESPONSE
902.33
UV_RESPONSE_DN
3025.71
UV_RESPONSE_UP
1988.08
WNT_BETA_CATENIN_SIGNALING
1506.90
XENOBIOTIC_METABOLISM
771.15

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 = 0.863

SampleCancer typecos to ideal
EPT0291EPN0.863
TCGA-CF-A5U8-01A-11R-A28M-070.846
SRR1443713GTEX0.842
SRR122024980.841
SRR1311182GTEX0.824

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