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

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

Selectivity scorecard

MeasuredDerived
KISS
93.23
Gini
0.688
CATDS
0.012

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 Axitinib. Strongest target: AURORA_A at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1AURORA_A100.0%0.0%
2ABL199.4%0.6%
3TNIK99.0%1.0%
4FLT4_VEGFR398.5%1.5%
5ABL2_ARG98.3%1.7%
6FLT1_VEGFR198.1%1.9%
7KDR_VEGFR296.9%3.1%
8FGFR296.1%3.9%
9PDGFRA96.0%4.0%
10FMS95.2%4.8%
11AURORA_B95.1%4.9%
12FGFR194.9%5.1%
13ROS_ROS193.7%6.3%
14AMPK(A1_B2_G2)93.7%6.3%
15AMPK(A1_B2_G3)93.6%6.4%
16MINK_MINK193.4%6.6%
17AMPK(A1_B2_G1)93.3%6.7%
18FGFR393.1%6.9%
19AMPK(A2_B2_G2)93.0%7.0%
20PDGFRB92.9%7.1%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Axitinib

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
2116.56
ALLOGRAFT_REJECTION
7428.81
ANDROGEN_RESPONSE
1307.05
ANGIOGENESIS
1437.60
APICAL_JUNCTION
7944.24
APICAL_SURFACE
860.23
APOPTOSIS
6343.31
BILE_ACID_METABOLISM
827.68
CHOLESTEROL_HOMEOSTASIS
1258.94
COAGULATION
850.30
COMPLEMENT
4229.88
DNA_REPAIR
1424.21
E2F_TARGETS
3198.44
EPITHELIAL_MESENCHYMAL_TRANSITION
1616.69
ESTROGEN_RESPONSE_EARLY
2594.29
ESTROGEN_RESPONSE_LATE
2579.14
FATTY_ACID_METABOLISM
869.28
G2M_CHECKPOINT
3347.80
GLYCOLYSIS
2256.79
HEDGEHOG_SIGNALING
636.77
HEME_METABOLISM
1802.49
HYPOXIA
3341.37
IL2_STAT5_SIGNALING
2334.08
IL6_JAK_STAT3_SIGNALING
4504.90
INFLAMMATORY_RESPONSE
3426.59
INTERFERON_ALPHA_RESPONSE
730.68
INTERFERON_GAMMA_RESPONSE
5098.27
KRAS_SIGNALING_DN
774.09
KRAS_SIGNALING_UP
2780.26
MITOTIC_SPINDLE
5272.44
MTORC1_SIGNALING
3005.45
MYC_TARGETS_V1
2193.69
MYC_TARGETS_V2
569.26
MYOGENESIS
2464.23
NOTCH_SIGNALING
172.57
OXIDATIVE_PHOSPHORYLATION
1393.93
P53_PATHWAY
2939.43
PANCREAS_BETA_CELLS
217.43
PEROXISOME
1139.41
PI3K_AKT_MTOR_SIGNALING
8166.36
PROTEIN_SECRETION
1838.77
REACTIVE_OXYGEN_SPECIES_PATHWAY
377.15
SPERMATOGENESIS
992.54
TGF_BETA_SIGNALING
1633.14
TNFA_SIGNALING_VIA_NFKB
3370.13
UNFOLDED_PROTEIN_RESPONSE
1138.09
UV_RESPONSE_DN
3957.32
UV_RESPONSE_UP
2915.49
WNT_BETA_CATENIN_SIGNALING
1524.41
XENOBIOTIC_METABOLISM
1635.78

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 = 3.10 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 = 0.829

SampleCancer typecos to ideal
SRR233037520.829
EPT0291EPN0.825
SRR108999840.814
aMVAC.P_005_TURBT_S2230.810
SRR122024980.802

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