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

Primary targets: PDGFRA, PDGFRB · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
97.73
Gini
0.644
CATDS
0.016

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 Avapritinib. Strongest target: PDGFRA at 99.1% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1PDGFRA99.1%0.9%
2C_KIT98.8%1.2%
3LIMK198.4%1.6%
4DDR196.0%4.0%
5FMS95.9%4.1%
6LCK92.7%7.3%
7LYN91.4%8.6%
8RET90.4%9.6%
9PDGFRB90.4%9.6%
10NEK589.7%10.3%
11FLT388.6%11.4%
12LIMK285.0%15.0%
13FGR80.0%20.0%
14BLK79.3%20.7%
15YES_YES178.7%21.3%
16NEK178.7%21.3%
17FLT4_VEGFR376.0%24.0%
18ABL175.1%24.9%
19ERBB2_HER275.1%24.9%
20CLK172.4%27.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Avapritinib

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
2135.12
ALLOGRAFT_REJECTION
6909.77
ANDROGEN_RESPONSE
1197.89
ANGIOGENESIS
1135.83
APICAL_JUNCTION
7383.36
APICAL_SURFACE
575.80
APOPTOSIS
5018.59
BILE_ACID_METABOLISM
682.32
CHOLESTEROL_HOMEOSTASIS
939.70
COAGULATION
945.96
COMPLEMENT
4185.30
DNA_REPAIR
1436.77
E2F_TARGETS
3409.15
EPITHELIAL_MESENCHYMAL_TRANSITION
1492.51
ESTROGEN_RESPONSE_EARLY
2109.66
ESTROGEN_RESPONSE_LATE
2149.35
FATTY_ACID_METABOLISM
682.74
G2M_CHECKPOINT
3908.09
GLYCOLYSIS
1977.16
HEDGEHOG_SIGNALING
718.97
HEME_METABOLISM
1701.90
HYPOXIA
3164.50
IL2_STAT5_SIGNALING
2344.72
IL6_JAK_STAT3_SIGNALING
4124.34
INFLAMMATORY_RESPONSE
3693.28
INTERFERON_ALPHA_RESPONSE
577.08
INTERFERON_GAMMA_RESPONSE
4819.13
KRAS_SIGNALING_DN
575.15
KRAS_SIGNALING_UP
2988.33
MITOTIC_SPINDLE
4891.20
MTORC1_SIGNALING
2888.53
MYC_TARGETS_V1
2676.98
MYC_TARGETS_V2
667.66
MYOGENESIS
2123.72
NOTCH_SIGNALING
280.76
OXIDATIVE_PHOSPHORYLATION
1088.20
P53_PATHWAY
2658.27
PANCREAS_BETA_CELLS
268.28
PEROXISOME
948.50
PI3K_AKT_MTOR_SIGNALING
6864.59
PROTEIN_SECRETION
1247.81
REACTIVE_OXYGEN_SPECIES_PATHWAY
435.05
SPERMATOGENESIS
1133.89
TGF_BETA_SIGNALING
1426.41
TNFA_SIGNALING_VIA_NFKB
3383.64
UNFOLDED_PROTEIN_RESPONSE
1196.36
UV_RESPONSE_DN
3532.57
UV_RESPONSE_UP
2755.60
WNT_BETA_CATENIN_SIGNALING
1444.24
XENOBIOTIC_METABOLISM
1212.30

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
SRR233037520.832
TCGA-CF-A5U8-01A-11R-A28M-070.826
aMVAC.P_005_TURBT_S2230.821
SRR108999840.819

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