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

Primary targets: KDR_VEGFR2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
91.73
Gini
0.524
CATDS
0.007

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 Sunitinib. Strongest target: CAMK2D at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1CAMK2D100.0%0.0%
2MYLK499.1%0.9%
3FLT398.7%1.3%
4TNIK98.3%1.7%
5ARK5_NUAK197.8%2.2%
6KHS_MAP4K597.8%2.2%
7GLK_MAP4K397.6%2.4%
8RET97.2%2.8%
9FMS97.1%2.9%
10YES_YES196.6%3.4%
11CAMK2A96.3%3.7%
12HPK1_MAP4K196.3%3.7%
13AMPK(A2_B2_G2)96.3%3.7%
14LRRK295.8%4.2%
15PHKG195.6%4.4%
16TRKC95.4%4.6%
17CHK295.0%5.0%
18AMPK(A1_B2_G1)94.6%5.4%
19AMPK(A1_B2_G2)94.5%5.5%
20AMPK(A1_B2_G3)93.6%6.4%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Sunitinib

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
3155.87
ALLOGRAFT_REJECTION
10247.27
ANDROGEN_RESPONSE
2348.88
ANGIOGENESIS
1800.49
APICAL_JUNCTION
10768.75
APICAL_SURFACE
986.03
APOPTOSIS
8948.13
BILE_ACID_METABOLISM
1236.89
CHOLESTEROL_HOMEOSTASIS
1388.75
COAGULATION
1164.98
COMPLEMENT
5922.98
DNA_REPAIR
2268.04
E2F_TARGETS
6500.87
EPITHELIAL_MESENCHYMAL_TRANSITION
2977.58
ESTROGEN_RESPONSE_EARLY
4517.89
ESTROGEN_RESPONSE_LATE
4335.13
FATTY_ACID_METABOLISM
887.26
G2M_CHECKPOINT
6464.53
GLYCOLYSIS
4125.20
HEDGEHOG_SIGNALING
1349.20
HEME_METABOLISM
2587.29
HYPOXIA
5437.55
IL2_STAT5_SIGNALING
3295.50
IL6_JAK_STAT3_SIGNALING
6426.01
INFLAMMATORY_RESPONSE
5384.35
INTERFERON_ALPHA_RESPONSE
890.46
INTERFERON_GAMMA_RESPONSE
7648.24
KRAS_SIGNALING_DN
1587.59
KRAS_SIGNALING_UP
3789.64
MITOTIC_SPINDLE
7686.19
MTORC1_SIGNALING
4974.54
MYC_TARGETS_V1
3896.58
MYC_TARGETS_V2
984.68
MYOGENESIS
4756.31
NOTCH_SIGNALING
338.09
OXIDATIVE_PHOSPHORYLATION
1581.66
P53_PATHWAY
4711.77
PANCREAS_BETA_CELLS
552.82
PEROXISOME
1667.51
PI3K_AKT_MTOR_SIGNALING
11320.05
PROTEIN_SECRETION
2557.47
REACTIVE_OXYGEN_SPECIES_PATHWAY
534.35
SPERMATOGENESIS
2006.43
TGF_BETA_SIGNALING
2618.16
TNFA_SIGNALING_VIA_NFKB
5455.97
UNFOLDED_PROTEIN_RESPONSE
2104.51
UV_RESPONSE_DN
5894.09
UV_RESPONSE_UP
4767.33
WNT_BETA_CATENIN_SIGNALING
2813.20
XENOBIOTIC_METABOLISM
2480.78

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 = 0.850

SampleCancer typecos to ideal
EPT0291EPN0.850
SRR233037520.836
TCGA-CF-A5U8-01A-11R-A28M-070.833
aMVAC.P_005_TURBT_S2230.824
SRR108999840.823

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