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

Primary targets: FLT1_VEGFR1, FLT4_VEGFR3, KDR_VEGFR2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
96.72
Gini
0.776
CATDS
0.023

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 Sorafenib. Strongest target: RAF1 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1RAF1100.0%0.0%
2ARAF100.0%0.0%
3BRAF98.5%1.5%
4HIPK498.5%1.5%
5C_KIT98.2%1.8%
6FMS98.1%1.9%
7FLT397.3%2.6%
8DDR296.3%3.7%
9YSK4_MAP3K1996.3%3.7%
10PDGFRA95.6%4.4%
11DDR194.2%5.8%
12RET94.0%6.0%
13MUSK92.0%8.0%
14FLT1_VEGFR189.5%10.5%
15FLT4_VEGFR387.6%12.4%
16ZAK_MLTK86.2%13.8%
17PDGFRB80.8%19.1%
18TAOK2_TAO180.8%19.2%
19ERK7_MAPK1579.1%20.9%
20KDR_VEGFR278.4%21.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Sorafenib

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
1179.22
ALLOGRAFT_REJECTION
2566.85
ANDROGEN_RESPONSE
543.76
ANGIOGENESIS
575.48
APICAL_JUNCTION
3819.81
APICAL_SURFACE
291.78
APOPTOSIS
2672.41
BILE_ACID_METABOLISM
467.87
CHOLESTEROL_HOMEOSTASIS
626.11
COAGULATION
360.42
COMPLEMENT
1902.37
DNA_REPAIR
740.14
E2F_TARGETS
2015.22
EPITHELIAL_MESENCHYMAL_TRANSITION
905.94
ESTROGEN_RESPONSE_EARLY
1348.49
ESTROGEN_RESPONSE_LATE
1256.03
FATTY_ACID_METABOLISM
438.43
G2M_CHECKPOINT
1986.41
GLYCOLYSIS
1065.65
HEDGEHOG_SIGNALING
455.10
HEME_METABOLISM
807.10
HYPOXIA
1477.36
IL2_STAT5_SIGNALING
990.66
IL6_JAK_STAT3_SIGNALING
1752.70
INFLAMMATORY_RESPONSE
1572.82
INTERFERON_ALPHA_RESPONSE
289.58
INTERFERON_GAMMA_RESPONSE
1843.47
KRAS_SIGNALING_DN
441.08
KRAS_SIGNALING_UP
1226.99
MITOTIC_SPINDLE
2530.20
MTORC1_SIGNALING
1362.62
MYC_TARGETS_V1
1449.57
MYC_TARGETS_V2
322.45
MYOGENESIS
1060.06
NOTCH_SIGNALING
58.78
OXIDATIVE_PHOSPHORYLATION
919.72
P53_PATHWAY
1199.66
PANCREAS_BETA_CELLS
117.87
PEROXISOME
531.67
PI3K_AKT_MTOR_SIGNALING
4072.19
PROTEIN_SECRETION
801.46
REACTIVE_OXYGEN_SPECIES_PATHWAY
166.80
SPERMATOGENESIS
696.67
TGF_BETA_SIGNALING
854.02
TNFA_SIGNALING_VIA_NFKB
1665.26
UNFOLDED_PROTEIN_RESPONSE
623.50
UV_RESPONSE_DN
2213.79
UV_RESPONSE_UP
1258.18
WNT_BETA_CATENIN_SIGNALING
936.32
XENOBIOTIC_METABOLISM
709.43

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 = 3.14 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 = 0.831

SampleCancer typecos to ideal
SRR233037520.831
EPT0291EPN0.831
aMVAC.P_005_TURBT_S2230.813
TCGA-CF-A5U8-01A-11R-A28M-070.810
SRR122024980.805

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