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

Primary targets: RET, KDR_VEGFR2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
92.73
Gini
0.751
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 Cabozantinib. Strongest target: DDR2 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1DDR2100.0%0.0%
2TRKB100.0%0.0%
3DDR1100.0%0.0%
4HIPK4100.0%0.0%
5BRK99.5%0.5%
6C_MET99.2%0.8%
7RET97.5%2.5%
8LCK97.5%2.5%
9C_MER97.0%3.0%
10YSK4_MAP3K1996.8%3.2%
11ROS_ROS196.0%4.0%
12AXL95.9%4.1%
13EPHA695.7%4.3%
14FLT4_VEGFR395.2%4.8%
15KDR_VEGFR295.0%5.0%
16FLT395.0%5.0%
17RIPK394.5%5.5%
18EPHB294.5%5.5%
19EPHA494.5%5.5%
20LOK_STK1094.3%5.7%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Cabozantinib

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
1849.27
ALLOGRAFT_REJECTION
6752.63
ANDROGEN_RESPONSE
969.71
ANGIOGENESIS
1275.34
APICAL_JUNCTION
7124.76
APICAL_SURFACE
612.34
APOPTOSIS
4527.96
BILE_ACID_METABOLISM
761.85
CHOLESTEROL_HOMEOSTASIS
809.27
COAGULATION
863.09
COMPLEMENT
3753.94
DNA_REPAIR
1118.98
E2F_TARGETS
2413.55
EPITHELIAL_MESENCHYMAL_TRANSITION
1161.51
ESTROGEN_RESPONSE_EARLY
1774.18
ESTROGEN_RESPONSE_LATE
1750.44
FATTY_ACID_METABOLISM
603.65
G2M_CHECKPOINT
2860.62
GLYCOLYSIS
1786.54
HEDGEHOG_SIGNALING
810.04
HEME_METABOLISM
1333.16
HYPOXIA
2506.67
IL2_STAT5_SIGNALING
1920.39
IL6_JAK_STAT3_SIGNALING
3313.71
INFLAMMATORY_RESPONSE
2899.84
INTERFERON_ALPHA_RESPONSE
476.39
INTERFERON_GAMMA_RESPONSE
3743.27
KRAS_SIGNALING_DN
360.49
KRAS_SIGNALING_UP
2386.31
MITOTIC_SPINDLE
4035.29
MTORC1_SIGNALING
2448.50
MYC_TARGETS_V1
1926.93
MYC_TARGETS_V2
344.54
MYOGENESIS
1657.97
NOTCH_SIGNALING
120.32
OXIDATIVE_PHOSPHORYLATION
1103.64
P53_PATHWAY
2088.73
PANCREAS_BETA_CELLS
136.81
PEROXISOME
723.94
PI3K_AKT_MTOR_SIGNALING
6076.40
PROTEIN_SECRETION
1080.14
REACTIVE_OXYGEN_SPECIES_PATHWAY
385.18
SPERMATOGENESIS
697.18
TGF_BETA_SIGNALING
1088.33
TNFA_SIGNALING_VIA_NFKB
2578.95
UNFOLDED_PROTEIN_RESPONSE
851.70
UV_RESPONSE_DN
3031.29
UV_RESPONSE_UP
2454.53
WNT_BETA_CATENIN_SIGNALING
1103.09
XENOBIOTIC_METABOLISM
1141.38

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 = 0.818

SampleCancer typecos to ideal
SRR233037520.818
EPT0291EPN0.809
SRR108999840.802
aMVAC.P_005_TURBT_S2230.798
TCGA-CF-A5U8-01A-11R-A28M-070.794

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