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

Primary targets: ALK, ROS_ROS1 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
91.39
Gini
0.581
CATDS
0.009

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 Crizotinib. Strongest target: EPHA6 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1EPHA6100.0%0.0%
2ROS_ROS1100.0%0.0%
3RON_MST1R99.8%0.2%
4LIMK198.9%1.1%
5JAK298.7%1.3%
6TRKB98.5%1.5%
7TYK1_LTK98.3%1.7%
8HPK1_MAP4K197.9%2.1%
9ALK97.7%2.3%
10MUSK97.7%2.3%
11TRKC97.3%2.7%
12AXL97.1%2.9%
13ABL197.0%3.0%
14LCK96.8%3.2%
15EPHB196.8%3.2%
16C_MET96.7%3.3%
17ARK5_NUAK196.4%3.6%
18EPHA296.0%4.0%
19TRKA95.8%4.2%
20FAK_PTK295.7%4.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Crizotinib

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
2894.19
ALLOGRAFT_REJECTION
9752.38
ANDROGEN_RESPONSE
1405.54
ANGIOGENESIS
1502.50
APICAL_JUNCTION
9109.49
APICAL_SURFACE
1025.67
APOPTOSIS
6329.09
BILE_ACID_METABOLISM
926.38
CHOLESTEROL_HOMEOSTASIS
1202.01
COAGULATION
1195.43
COMPLEMENT
5694.69
DNA_REPAIR
1679.91
E2F_TARGETS
4000.78
EPITHELIAL_MESENCHYMAL_TRANSITION
1822.43
ESTROGEN_RESPONSE_EARLY
3233.88
ESTROGEN_RESPONSE_LATE
2999.54
FATTY_ACID_METABOLISM
739.61
G2M_CHECKPOINT
4352.92
GLYCOLYSIS
2689.26
HEDGEHOG_SIGNALING
997.00
HEME_METABOLISM
2158.70
HYPOXIA
4182.10
IL2_STAT5_SIGNALING
3661.12
IL6_JAK_STAT3_SIGNALING
6495.40
INFLAMMATORY_RESPONSE
5290.61
INTERFERON_ALPHA_RESPONSE
893.79
INTERFERON_GAMMA_RESPONSE
7244.00
KRAS_SIGNALING_DN
958.57
KRAS_SIGNALING_UP
3434.46
MITOTIC_SPINDLE
5986.05
MTORC1_SIGNALING
3808.45
MYC_TARGETS_V1
2859.95
MYC_TARGETS_V2
910.13
MYOGENESIS
2889.61
NOTCH_SIGNALING
215.03
OXIDATIVE_PHOSPHORYLATION
1167.52
P53_PATHWAY
3735.47
PANCREAS_BETA_CELLS
269.26
PEROXISOME
1067.82
PI3K_AKT_MTOR_SIGNALING
9119.10
PROTEIN_SECRETION
1696.07
REACTIVE_OXYGEN_SPECIES_PATHWAY
509.13
SPERMATOGENESIS
1530.90
TGF_BETA_SIGNALING
1762.50
TNFA_SIGNALING_VIA_NFKB
4527.56
UNFOLDED_PROTEIN_RESPONSE
1392.88
UV_RESPONSE_DN
4866.48
UV_RESPONSE_UP
4009.65
WNT_BETA_CATENIN_SIGNALING
1769.28
XENOBIOTIC_METABOLISM
1846.55

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 = 3.06 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 = 0.835

SampleCancer typecos to ideal
EPT0291EPN0.835
SRR233037520.831
SRR108999840.826
TCGA-CF-A5U8-01A-11R-A28M-070.818
aMVAC.P_005_TURBT_S2230.816

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