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
92.42
Gini
0.673
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 Tivozanib. Strongest target: RET at 99.7% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1RET99.7%0.3%
2C_KIT99.4%0.6%
3KDR_VEGFR299.3%0.7%
4FLT4_VEGFR399.3%0.7%
5LYN99.3%0.7%
6DDR299.3%0.7%
7FMS98.6%1.4%
8EPHA698.3%1.7%
9EPHB298.0%2.0%
10C_MET97.7%2.4%
11FLT1_VEGFR197.6%2.4%
12LCK97.5%2.5%
13BRK97.2%2.8%
14FRK_PTK597.2%2.8%
15HCK97.1%2.9%
16DDR197.1%2.9%
17PDGFRA96.9%3.1%
18FGR96.6%3.4%
19LOK_STK1096.2%3.8%
20TRKC96.1%3.9%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Tivozanib

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
2625.29
ALLOGRAFT_REJECTION
9325.30
ANDROGEN_RESPONSE
1351.13
ANGIOGENESIS
1793.42
APICAL_JUNCTION
9942.20
APICAL_SURFACE
1069.22
APOPTOSIS
6687.33
BILE_ACID_METABOLISM
1038.51
CHOLESTEROL_HOMEOSTASIS
1344.94
COAGULATION
1272.21
COMPLEMENT
5500.66
DNA_REPAIR
1537.00
E2F_TARGETS
3331.82
EPITHELIAL_MESENCHYMAL_TRANSITION
1595.73
ESTROGEN_RESPONSE_EARLY
2877.11
ESTROGEN_RESPONSE_LATE
2560.79
FATTY_ACID_METABOLISM
853.00
G2M_CHECKPOINT
3796.70
GLYCOLYSIS
2395.11
HEDGEHOG_SIGNALING
1068.51
HEME_METABOLISM
1945.63
HYPOXIA
4126.82
IL2_STAT5_SIGNALING
3226.32
IL6_JAK_STAT3_SIGNALING
5343.59
INFLAMMATORY_RESPONSE
4461.70
INTERFERON_ALPHA_RESPONSE
801.74
INTERFERON_GAMMA_RESPONSE
5942.37
KRAS_SIGNALING_DN
737.44
KRAS_SIGNALING_UP
3354.09
MITOTIC_SPINDLE
5949.12
MTORC1_SIGNALING
3372.61
MYC_TARGETS_V1
2617.14
MYC_TARGETS_V2
574.59
MYOGENESIS
2585.95
NOTCH_SIGNALING
188.59
OXIDATIVE_PHOSPHORYLATION
1463.84
P53_PATHWAY
3304.62
PANCREAS_BETA_CELLS
206.60
PEROXISOME
958.09
PI3K_AKT_MTOR_SIGNALING
9092.68
PROTEIN_SECRETION
1942.08
REACTIVE_OXYGEN_SPECIES_PATHWAY
513.16
SPERMATOGENESIS
1137.88
TGF_BETA_SIGNALING
1742.13
TNFA_SIGNALING_VIA_NFKB
3816.59
UNFOLDED_PROTEIN_RESPONSE
1133.76
UV_RESPONSE_DN
4894.81
UV_RESPONSE_UP
3486.49
WNT_BETA_CATENIN_SIGNALING
1581.44
XENOBIOTIC_METABOLISM
1802.77

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 = 0.823

SampleCancer typecos to ideal
SRR233037520.823
EPT0291EPN0.814
SRR108999840.809
aMVAC.P_005_TURBT_S2230.804
SRR122024980.798

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