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

Primary targets: BCR_ABL, ABL1, ABL2_ARG · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
99.00
Gini
0.718
CATDS
0.033

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 Imatinib. Strongest target: PDGFRA at 98.9% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1PDGFRA98.9%1.1%
2DDR194.5%5.5%
3FMS92.2%7.8%
4LCK90.2%9.8%
5DDR287.7%12.3%
6ABL186.2%13.8%
7LYN80.6%19.4%
8RAF174.0%26.0%
9PDGFRB70.7%29.3%
10ABL2_ARG63.1%36.9%
11C_KIT62.1%37.9%
12PDK2_PDHK243.2%56.8%
13ARAF42.8%57.2%
14BRAF39.8%60.2%
15ROS_ROS139.8%60.3%
16FGR38.9%61.1%
17CAMKK238.6%61.4%
18PKG2_PRKG231.0%69.0%
19BLK30.4%69.6%
20ERN1_IRE129.8%70.2%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Imatinib

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
1579.24
ALLOGRAFT_REJECTION
4874.01
ANDROGEN_RESPONSE
565.47
ANGIOGENESIS
794.23
APICAL_JUNCTION
5131.86
APICAL_SURFACE
425.95
APOPTOSIS
3665.05
BILE_ACID_METABOLISM
308.46
CHOLESTEROL_HOMEOSTASIS
764.16
COAGULATION
576.33
COMPLEMENT
2903.94
DNA_REPAIR
862.62
E2F_TARGETS
2208.38
EPITHELIAL_MESENCHYMAL_TRANSITION
1029.92
ESTROGEN_RESPONSE_EARLY
1686.28
ESTROGEN_RESPONSE_LATE
1497.37
FATTY_ACID_METABOLISM
276.42
G2M_CHECKPOINT
2309.36
GLYCOLYSIS
1220.97
HEDGEHOG_SIGNALING
421.26
HEME_METABOLISM
1101.81
HYPOXIA
1914.43
IL2_STAT5_SIGNALING
1856.09
IL6_JAK_STAT3_SIGNALING
2567.32
INFLAMMATORY_RESPONSE
2680.56
INTERFERON_ALPHA_RESPONSE
502.37
INTERFERON_GAMMA_RESPONSE
3288.25
KRAS_SIGNALING_DN
494.28
KRAS_SIGNALING_UP
1970.45
MITOTIC_SPINDLE
3648.46
MTORC1_SIGNALING
1754.97
MYC_TARGETS_V1
1887.35
MYC_TARGETS_V2
474.52
MYOGENESIS
1493.42
NOTCH_SIGNALING
106.81
OXIDATIVE_PHOSPHORYLATION
466.51
P53_PATHWAY
2066.96
PANCREAS_BETA_CELLS
159.02
PEROXISOME
640.32
PI3K_AKT_MTOR_SIGNALING
4445.30
PROTEIN_SECRETION
821.51
REACTIVE_OXYGEN_SPECIES_PATHWAY
325.84
SPERMATOGENESIS
884.33
TGF_BETA_SIGNALING
972.85
TNFA_SIGNALING_VIA_NFKB
2493.37
UNFOLDED_PROTEIN_RESPONSE
583.16
UV_RESPONSE_DN
2500.64
UV_RESPONSE_UP
1911.24
WNT_BETA_CATENIN_SIGNALING
941.61
XENOBIOTIC_METABOLISM
819.84

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 = 0.830

SampleCancer typecos to ideal
EPT0291EPN0.830
SRR233037520.824
TCGA-CF-A5U8-01A-11R-A28M-070.816
aMVAC.P_005_TURBT_S2230.812
SRR108999840.810

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