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
100.00
Gini
0.602
CATDS
0.022

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 Asciminib. Strongest target: ABL2_ARG at 30.7% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ABL2_ARG30.7%69.3%
2NEK1119.7%80.3%
3PDK2_PDHK216.7%83.3%
4ASK1_MAP3K516.4%83.6%
5AURORA_A15.3%84.7%
6MAPKAPK215.3%84.7%
7WNK314.9%85.1%
8ERK2_MAPK114.4%85.6%
9EPHA613.8%86.2%
10BMPR213.7%86.3%
11RIPK213.6%86.4%
12NEK413.5%86.5%
13ARAF13.1%86.9%
14PIM212.8%87.2%
15TRKB12.8%87.2%
16WNK112.4%87.6%
17MARK312.4%87.6%
18CDK17_CYCLIN_Y(PCTK2)12.3%87.7%
19ERN2_IRE212.2%87.8%
20SGK3_SGKL12.2%87.8%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Asciminib

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
349.79
ALLOGRAFT_REJECTION
798.30
ANDROGEN_RESPONSE
323.46
ANGIOGENESIS
85.36
APICAL_JUNCTION
822.96
APICAL_SURFACE
130.13
APOPTOSIS
1134.25
BILE_ACID_METABOLISM
114.77
CHOLESTEROL_HOMEOSTASIS
149.05
COAGULATION
88.79
COMPLEMENT
495.43
DNA_REPAIR
273.00
E2F_TARGETS
1065.90
EPITHELIAL_MESENCHYMAL_TRANSITION
314.23
ESTROGEN_RESPONSE_EARLY
576.97
ESTROGEN_RESPONSE_LATE
500.97
FATTY_ACID_METABOLISM
82.75
G2M_CHECKPOINT
952.45
GLYCOLYSIS
389.05
HEDGEHOG_SIGNALING
58.50
HEME_METABOLISM
310.60
HYPOXIA
747.73
IL2_STAT5_SIGNALING
435.97
IL6_JAK_STAT3_SIGNALING
540.22
INFLAMMATORY_RESPONSE
570.03
INTERFERON_ALPHA_RESPONSE
100.64
INTERFERON_GAMMA_RESPONSE
740.82
KRAS_SIGNALING_DN
173.23
KRAS_SIGNALING_UP
301.17
MITOTIC_SPINDLE
762.32
MTORC1_SIGNALING
535.27
MYC_TARGETS_V1
620.16
MYC_TARGETS_V2
183.20
MYOGENESIS
545.66
NOTCH_SIGNALING
63.43
OXIDATIVE_PHOSPHORYLATION
110.59
P53_PATHWAY
682.49
PANCREAS_BETA_CELLS
90.62
PEROXISOME
172.18
PI3K_AKT_MTOR_SIGNALING
1137.99
PROTEIN_SECRETION
265.09
REACTIVE_OXYGEN_SPECIES_PATHWAY
88.70
SPERMATOGENESIS
297.20
TGF_BETA_SIGNALING
351.10
TNFA_SIGNALING_VIA_NFKB
745.48
UNFOLDED_PROTEIN_RESPONSE
274.32
UV_RESPONSE_DN
665.22
UV_RESPONSE_UP
530.39
WNT_BETA_CATENIN_SIGNALING
362.72
XENOBIOTIC_METABOLISM
257.23

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 = 0.873

SampleCancer typecos to ideal
EPT0291EPN0.873
TCGA-CF-A5U8-01A-11R-A28M-070.849
SRR122024980.838
SRR1443713GTEX0.836
R2470.830

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