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
97.49
Gini
0.672
CATDS
0.014

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 Pazopanib. Strongest target: FLT4_VEGFR3 at 96.1% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1FLT4_VEGFR396.1%3.9%
2TNIK95.8%4.2%
3RAF195.5%4.5%
4MLK3_MAP3K1194.2%5.8%
5FLT1_VEGFR193.0%7.0%
6FMS93.0%7.0%
7KDR_VEGFR292.8%7.2%
8MLK1_MAP3K992.5%7.5%
9DDR191.8%8.2%
10ROS_ROS191.4%8.6%
11LIMK289.2%10.8%
12FGFR288.9%11.1%
13LYN88.5%11.5%
14FGFR187.3%12.7%
15LCK87.0%13.0%
16DDR286.1%13.9%
17MLK2_MAP3K1084.8%15.2%
18RET83.8%16.2%
19RIPK382.2%17.8%
20LIMK181.1%18.9%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Pazopanib

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
2414.54
ALLOGRAFT_REJECTION
7298.94
ANDROGEN_RESPONSE
1557.96
ANGIOGENESIS
1255.87
APICAL_JUNCTION
7875.65
APICAL_SURFACE
693.89
APOPTOSIS
5673.15
BILE_ACID_METABOLISM
763.70
CHOLESTEROL_HOMEOSTASIS
1194.61
COAGULATION
858.86
COMPLEMENT
4505.80
DNA_REPAIR
1546.05
E2F_TARGETS
3753.84
EPITHELIAL_MESENCHYMAL_TRANSITION
1800.83
ESTROGEN_RESPONSE_EARLY
2590.34
ESTROGEN_RESPONSE_LATE
2466.63
FATTY_ACID_METABOLISM
903.59
G2M_CHECKPOINT
3852.26
GLYCOLYSIS
2315.13
HEDGEHOG_SIGNALING
724.17
HEME_METABOLISM
1760.69
HYPOXIA
3187.15
IL2_STAT5_SIGNALING
2521.64
IL6_JAK_STAT3_SIGNALING
4285.99
INFLAMMATORY_RESPONSE
3927.86
INTERFERON_ALPHA_RESPONSE
732.56
INTERFERON_GAMMA_RESPONSE
5042.61
KRAS_SIGNALING_DN
951.01
KRAS_SIGNALING_UP
3054.21
MITOTIC_SPINDLE
5416.81
MTORC1_SIGNALING
3196.94
MYC_TARGETS_V1
3133.18
MYC_TARGETS_V2
734.83
MYOGENESIS
2407.19
NOTCH_SIGNALING
286.87
OXIDATIVE_PHOSPHORYLATION
1403.25
P53_PATHWAY
2950.11
PANCREAS_BETA_CELLS
279.70
PEROXISOME
1079.39
PI3K_AKT_MTOR_SIGNALING
8161.90
PROTEIN_SECRETION
1730.86
REACTIVE_OXYGEN_SPECIES_PATHWAY
459.34
SPERMATOGENESIS
1271.33
TGF_BETA_SIGNALING
1746.49
TNFA_SIGNALING_VIA_NFKB
3723.96
UNFOLDED_PROTEIN_RESPONSE
1188.06
UV_RESPONSE_DN
4224.20
UV_RESPONSE_UP
3081.50
WNT_BETA_CATENIN_SIGNALING
1785.42
XENOBIOTIC_METABOLISM
1609.98

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 = 3.11 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 = 0.840

SampleCancer typecos to ideal
EPT0291EPN0.840
SRR233037520.838
aMVAC.P_005_TURBT_S2230.823
TCGA-CF-A5U8-01A-11R-A28M-070.820
SRR122024980.818

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