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
95.74
Gini
0.723
CATDS
0.016

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 Vandetanib. Strongest target: EGFR at 99.3% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1EGFR99.3%0.7%
2LCK98.9%1.1%
3RET98.6%1.4%
4DDR298.5%1.5%
5DDR198.5%1.5%
6LYN98.0%2.0%
7EPHA697.3%2.7%
8ABL195.7%4.3%
9BRK95.3%4.7%
10YES_YES195.2%4.8%
11FLT4_VEGFR394.8%5.2%
12KDR_VEGFR294.5%5.5%
13PEAK194.4%5.6%
14C_SRC94.2%5.8%
15LOK_STK1093.8%6.2%
16BLK92.8%7.2%
17FGFR290.8%9.2%
18ABL2_ARG89.0%11.0%
19FLT1_VEGFR188.6%11.4%
20EPHB188.1%11.9%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Vandetanib

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
2493.47
ALLOGRAFT_REJECTION
8873.12
ANDROGEN_RESPONSE
1597.35
ANGIOGENESIS
1823.91
APICAL_JUNCTION
10177.71
APICAL_SURFACE
1052.28
APOPTOSIS
6909.58
BILE_ACID_METABOLISM
1002.99
CHOLESTEROL_HOMEOSTASIS
1715.36
COAGULATION
1141.26
COMPLEMENT
5706.60
DNA_REPAIR
1757.27
E2F_TARGETS
3382.48
EPITHELIAL_MESENCHYMAL_TRANSITION
1696.15
ESTROGEN_RESPONSE_EARLY
2507.71
ESTROGEN_RESPONSE_LATE
2411.36
FATTY_ACID_METABOLISM
914.45
G2M_CHECKPOINT
3573.10
GLYCOLYSIS
2638.70
HEDGEHOG_SIGNALING
1067.26
HEME_METABOLISM
1858.67
HYPOXIA
3955.20
IL2_STAT5_SIGNALING
2922.59
IL6_JAK_STAT3_SIGNALING
4665.89
INFLAMMATORY_RESPONSE
4660.88
INTERFERON_ALPHA_RESPONSE
884.68
INTERFERON_GAMMA_RESPONSE
5672.30
KRAS_SIGNALING_DN
896.47
KRAS_SIGNALING_UP
3694.69
MITOTIC_SPINDLE
6469.03
MTORC1_SIGNALING
3622.70
MYC_TARGETS_V1
2790.57
MYC_TARGETS_V2
520.17
MYOGENESIS
2813.46
NOTCH_SIGNALING
219.73
OXIDATIVE_PHOSPHORYLATION
1632.85
P53_PATHWAY
3476.87
PANCREAS_BETA_CELLS
163.24
PEROXISOME
1110.40
PI3K_AKT_MTOR_SIGNALING
8576.33
PROTEIN_SECRETION
2090.64
REACTIVE_OXYGEN_SPECIES_PATHWAY
587.92
SPERMATOGENESIS
1035.15
TGF_BETA_SIGNALING
1705.05
TNFA_SIGNALING_VIA_NFKB
3649.18
UNFOLDED_PROTEIN_RESPONSE
998.40
UV_RESPONSE_DN
4648.74
UV_RESPONSE_UP
3465.38
WNT_BETA_CATENIN_SIGNALING
1840.01
XENOBIOTIC_METABOLISM
2182.16

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 = 0.828

SampleCancer typecos to ideal
SRR233037520.828
EPT0291EPN0.818
SRR108999840.812
aMVAC.P_005_TURBT_S2230.808
SRR122024980.801

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