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
87.97
Gini
0.699
CATDS
0.012

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 Dasatinib. Strongest target: ABL2_ARG at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ABL2_ARG100.0%0.0%
2BLK100.0%0.0%
3EPHA3100.0%0.0%
4EPHA5100.0%0.0%
5FYN100.0%0.0%
6LCK100.0%0.0%
7YES_YES1100.0%0.0%
8C_SRC100.0%0.0%
9PEAK199.9%0.1%
10HCK99.9%0.1%
11DDR299.6%0.4%
12LYN99.6%0.4%
13FRK_PTK599.5%0.5%
14EPHA299.4%0.6%
15EPHB199.4%0.6%
16DDR199.3%0.7%
17BTK99.3%0.7%
18EPHB499.3%0.7%
19TXK99.1%0.9%
20EPHA198.9%1.1%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Dasatinib

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
3030.69
ALLOGRAFT_REJECTION
10882.35
ANDROGEN_RESPONSE
2018.74
ANGIOGENESIS
1997.74
APICAL_JUNCTION
11616.36
APICAL_SURFACE
1261.56
APOPTOSIS
8060.76
BILE_ACID_METABOLISM
1172.32
CHOLESTEROL_HOMEOSTASIS
1811.97
COAGULATION
1464.31
COMPLEMENT
7156.86
DNA_REPAIR
2135.65
E2F_TARGETS
4482.05
EPITHELIAL_MESENCHYMAL_TRANSITION
2130.15
ESTROGEN_RESPONSE_EARLY
3655.83
ESTROGEN_RESPONSE_LATE
3166.68
FATTY_ACID_METABOLISM
983.50
G2M_CHECKPOINT
4593.56
GLYCOLYSIS
2757.24
HEDGEHOG_SIGNALING
1286.09
HEME_METABOLISM
2255.91
HYPOXIA
4854.71
IL2_STAT5_SIGNALING
4003.50
IL6_JAK_STAT3_SIGNALING
5775.42
INFLAMMATORY_RESPONSE
6066.25
INTERFERON_ALPHA_RESPONSE
1094.21
INTERFERON_GAMMA_RESPONSE
6940.43
KRAS_SIGNALING_DN
1075.47
KRAS_SIGNALING_UP
4394.76
MITOTIC_SPINDLE
7475.08
MTORC1_SIGNALING
4056.77
MYC_TARGETS_V1
3270.53
MYC_TARGETS_V2
637.98
MYOGENESIS
3538.14
NOTCH_SIGNALING
392.10
OXIDATIVE_PHOSPHORYLATION
1419.05
P53_PATHWAY
4236.36
PANCREAS_BETA_CELLS
267.37
PEROXISOME
1007.77
PI3K_AKT_MTOR_SIGNALING
10732.42
PROTEIN_SECRETION
2294.07
REACTIVE_OXYGEN_SPECIES_PATHWAY
684.08
SPERMATOGENESIS
1564.73
TGF_BETA_SIGNALING
2090.79
TNFA_SIGNALING_VIA_NFKB
4988.35
UNFOLDED_PROTEIN_RESPONSE
1223.03
UV_RESPONSE_DN
5885.73
UV_RESPONSE_UP
4481.78
WNT_BETA_CATENIN_SIGNALING
2292.97
XENOBIOTIC_METABOLISM
2237.16

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 = 3.10 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 = 0.829

SampleCancer typecos to ideal
SRR233037520.829
EPT0291EPN0.826
SRR108999840.815
aMVAC.P_005_TURBT_S2230.812
TCGA-CF-A5U8-01A-11R-A28M-070.810

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