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
98.24
Gini
0.788
CATDS
0.033

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 Zanubrutinib. Strongest target: ERBB4_HER4 at 99.6% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ERBB4_HER499.6%0.4%
2BMX_ETK99.3%0.7%
3BLK99.1%0.9%
4BTK97.4%2.6%
5TXK96.9%3.1%
6TEC95.8%4.2%
7BRK93.4%6.6%
8MEK289.9%10.1%
9FGR88.4%11.6%
10EGFR88.2%11.8%
11LCK87.3%12.7%
12YES_YES185.0%15.0%
13ITK74.5%25.4%
14CSK64.0%36.0%
15MEK154.1%45.9%
16SRMS54.0%46.0%
17FYN50.7%49.3%
18LYN50.3%49.7%
19FLT347.8%52.2%
20ERBB2_HER247.2%52.8%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Zanubrutinib

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-target4%
Off-target96%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
1379.62
ALLOGRAFT_REJECTION
6405.15
ANDROGEN_RESPONSE
1159.79
ANGIOGENESIS
1151.91
APICAL_JUNCTION
6065.27
APICAL_SURFACE
648.98
APOPTOSIS
3895.94
BILE_ACID_METABOLISM
740.03
CHOLESTEROL_HOMEOSTASIS
874.88
COAGULATION
677.05
COMPLEMENT
3663.19
DNA_REPAIR
935.45
E2F_TARGETS
1894.87
EPITHELIAL_MESENCHYMAL_TRANSITION
1079.82
ESTROGEN_RESPONSE_EARLY
1501.92
ESTROGEN_RESPONSE_LATE
1320.47
FATTY_ACID_METABOLISM
514.09
G2M_CHECKPOINT
1970.81
GLYCOLYSIS
1298.19
HEDGEHOG_SIGNALING
488.05
HEME_METABOLISM
1101.43
HYPOXIA
2232.12
IL2_STAT5_SIGNALING
2002.27
IL6_JAK_STAT3_SIGNALING
2614.54
INFLAMMATORY_RESPONSE
3391.76
INTERFERON_ALPHA_RESPONSE
614.97
INTERFERON_GAMMA_RESPONSE
3684.23
KRAS_SIGNALING_DN
471.66
KRAS_SIGNALING_UP
2225.08
MITOTIC_SPINDLE
3557.77
MTORC1_SIGNALING
2409.99
MYC_TARGETS_V1
1328.80
MYC_TARGETS_V2
225.76
MYOGENESIS
1864.66
NOTCH_SIGNALING
178.28
OXIDATIVE_PHOSPHORYLATION
877.66
P53_PATHWAY
1932.71
PANCREAS_BETA_CELLS
69.06
PEROXISOME
516.76
PI3K_AKT_MTOR_SIGNALING
4905.13
PROTEIN_SECRETION
1278.77
REACTIVE_OXYGEN_SPECIES_PATHWAY
311.96
SPERMATOGENESIS
606.05
TGF_BETA_SIGNALING
824.61
TNFA_SIGNALING_VIA_NFKB
2430.00
UNFOLDED_PROTEIN_RESPONSE
608.20
UV_RESPONSE_DN
2405.04
UV_RESPONSE_UP
2174.58
WNT_BETA_CATENIN_SIGNALING
1096.88
XENOBIOTIC_METABOLISM
1431.98

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 = 3.07 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 = 0.821

SampleCancer typecos to ideal
SRR233037520.821
SRR108999840.813
EPT0291EPN0.810
TCGA-FD-A43X-01A-11R-A23W-070.804
SRR122024980.799

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