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
78.23
Gini
0.534
CATDS
0.007

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 Ponatinib. Strongest target: ABL1 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ABL1100.0%0.0%
2ABL2_ARG100.0%0.0%
3BLK100.0%0.0%
4C_KIT100.0%0.0%
5DDR2100.0%0.0%
6EPHA6100.0%0.0%
7FLT1_VEGFR1100.0%0.0%
8LYN100.0%0.0%
9LYN_B100.0%0.0%
10NEK4100.0%0.0%
11PDGFRB100.0%0.0%
12RAF1100.0%0.0%
13RET100.0%0.0%
14SRMS100.0%0.0%
15PDGFRA100.0%0.0%
16EPHB2100.0%0.0%
17C_SRC99.8%0.2%
18HCK99.8%0.2%
19FLT4_VEGFR399.8%0.2%
20HPK1_MAP4K199.7%0.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Ponatinib

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
3883.13
ALLOGRAFT_REJECTION
12429.44
ANDROGEN_RESPONSE
2571.43
ANGIOGENESIS
2368.01
APICAL_JUNCTION
13694.09
APICAL_SURFACE
1517.61
APOPTOSIS
9910.45
BILE_ACID_METABOLISM
1454.64
CHOLESTEROL_HOMEOSTASIS
2076.55
COAGULATION
1711.16
COMPLEMENT
7767.15
DNA_REPAIR
2532.55
E2F_TARGETS
6512.35
EPITHELIAL_MESENCHYMAL_TRANSITION
2482.40
ESTROGEN_RESPONSE_EARLY
4583.59
ESTROGEN_RESPONSE_LATE
4084.42
FATTY_ACID_METABOLISM
1212.01
G2M_CHECKPOINT
6749.84
GLYCOLYSIS
3622.54
HEDGEHOG_SIGNALING
1699.56
HEME_METABOLISM
2933.25
HYPOXIA
6167.43
IL2_STAT5_SIGNALING
4864.13
IL6_JAK_STAT3_SIGNALING
8402.27
INFLAMMATORY_RESPONSE
7616.16
INTERFERON_ALPHA_RESPONSE
1525.81
INTERFERON_GAMMA_RESPONSE
9703.83
KRAS_SIGNALING_DN
1519.53
KRAS_SIGNALING_UP
5073.67
MITOTIC_SPINDLE
8608.72
MTORC1_SIGNALING
5588.01
MYC_TARGETS_V1
4680.88
MYC_TARGETS_V2
1041.55
MYOGENESIS
4296.88
NOTCH_SIGNALING
353.13
OXIDATIVE_PHOSPHORYLATION
2178.32
P53_PATHWAY
5193.84
PANCREAS_BETA_CELLS
456.33
PEROXISOME
1259.09
PI3K_AKT_MTOR_SIGNALING
14060.45
PROTEIN_SECRETION
3132.30
REACTIVE_OXYGEN_SPECIES_PATHWAY
665.65
SPERMATOGENESIS
2308.89
TGF_BETA_SIGNALING
2840.37
TNFA_SIGNALING_VIA_NFKB
6512.54
UNFOLDED_PROTEIN_RESPONSE
1813.98
UV_RESPONSE_DN
7354.88
UV_RESPONSE_UP
4994.14
WNT_BETA_CATENIN_SIGNALING
2941.25
XENOBIOTIC_METABOLISM
2568.49

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 = 3.09 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 = 0.840

SampleCancer typecos to ideal
EPT0291EPN0.840
SRR233037520.835
TCGA-CF-A5U8-01A-11R-A28M-070.824
aMVAC.P_005_TURBT_S2230.823
SRR108999840.822

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