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

Primary targets: BTK · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
99.50
Gini
0.670
CATDS
0.044

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 Acalabrutinib. Strongest target: ERBB4_HER4 at 99.9% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ERBB4_HER499.9%0.1%
2BTK95.9%4.1%
3TEC87.4%12.6%
4BMX_ETK86.6%13.4%
5TXK58.7%41.3%
6ARAF58.3%41.7%
7BRK52.0%48.0%
8LIMK139.9%60.1%
9YES_YES139.9%60.1%
10CDK9_CYCLIN_T230.1%69.9%
11MEK324.2%75.8%
12RIPK223.3%76.7%
13ERN1_IRE120.1%79.9%
14BLK19.9%80.1%
15DDR119.1%80.9%
16AURORA_B17.9%82.1%
17PKCTHETA17.9%82.1%
18MKK617.6%82.4%
19CDK9_CYCLIN_T117.1%82.9%
20C_SRC16.9%83.1%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Acalabrutinib

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-target10%
Off-target90%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
501.36
ALLOGRAFT_REJECTION
1851.68
ANDROGEN_RESPONSE
414.92
ANGIOGENESIS
233.46
APICAL_JUNCTION
1680.57
APICAL_SURFACE
185.04
APOPTOSIS
1437.58
BILE_ACID_METABOLISM
164.95
CHOLESTEROL_HOMEOSTASIS
234.70
COAGULATION
217.32
COMPLEMENT
1141.80
DNA_REPAIR
560.75
E2F_TARGETS
1255.57
EPITHELIAL_MESENCHYMAL_TRANSITION
593.81
ESTROGEN_RESPONSE_EARLY
567.88
ESTROGEN_RESPONSE_LATE
521.14
FATTY_ACID_METABOLISM
129.85
G2M_CHECKPOINT
1146.63
GLYCOLYSIS
481.94
HEDGEHOG_SIGNALING
124.58
HEME_METABOLISM
438.40
HYPOXIA
807.70
IL2_STAT5_SIGNALING
704.35
IL6_JAK_STAT3_SIGNALING
700.22
INFLAMMATORY_RESPONSE
1223.68
INTERFERON_ALPHA_RESPONSE
156.74
INTERFERON_GAMMA_RESPONSE
1080.04
KRAS_SIGNALING_DN
215.65
KRAS_SIGNALING_UP
677.52
MITOTIC_SPINDLE
1492.03
MTORC1_SIGNALING
809.14
MYC_TARGETS_V1
806.83
MYC_TARGETS_V2
186.15
MYOGENESIS
866.24
NOTCH_SIGNALING
79.74
OXIDATIVE_PHOSPHORYLATION
233.73
P53_PATHWAY
788.98
PANCREAS_BETA_CELLS
71.69
PEROXISOME
183.79
PI3K_AKT_MTOR_SIGNALING
1865.80
PROTEIN_SECRETION
350.74
REACTIVE_OXYGEN_SPECIES_PATHWAY
95.40
SPERMATOGENESIS
417.59
TGF_BETA_SIGNALING
415.64
TNFA_SIGNALING_VIA_NFKB
1081.34
UNFOLDED_PROTEIN_RESPONSE
319.20
UV_RESPONSE_DN
814.17
UV_RESPONSE_UP
841.40
WNT_BETA_CATENIN_SIGNALING
554.08
XENOBIOTIC_METABOLISM
405.72

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 = 0.853

SampleCancer typecos to ideal
EPT0291EPN0.853
TCGA-CF-A5U8-01A-11R-A28M-070.849
SRR122024980.828
SRR233037520.828
SRR1443713GTEX0.827

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