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
94.74
Gini
0.723
CATDS
0.018

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 Ibrutinib. Strongest target: ERBB4_HER4 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1ERBB4_HER4100.0%0.0%
2TXK99.9%0.1%
3BLK99.7%0.3%
4EGFR99.3%0.7%
5CSK99.3%0.7%
6FGR99.1%0.9%
7BMX_ETK98.9%1.1%
8ERBB2_HER298.8%1.2%
9BTK98.8%1.3%
10TEC98.7%1.3%
11JAK398.6%1.4%
12LCK98.0%2.0%
13YES_YES196.5%3.5%
14BRK96.5%3.5%
15LYN95.7%4.3%
16HCK95.1%4.9%
17MKK794.8%5.2%
18CK2A294.7%5.3%
19ITK94.5%5.5%
20RIPK392.9%7.1%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Ibrutinib

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
2292.99
ALLOGRAFT_REJECTION
9523.08
ANDROGEN_RESPONSE
1843.22
ANGIOGENESIS
1761.76
APICAL_JUNCTION
9481.44
APICAL_SURFACE
986.75
APOPTOSIS
6236.80
BILE_ACID_METABOLISM
1025.39
CHOLESTEROL_HOMEOSTASIS
1495.04
COAGULATION
1092.75
COMPLEMENT
5430.17
DNA_REPAIR
1376.78
E2F_TARGETS
3160.09
EPITHELIAL_MESENCHYMAL_TRANSITION
1865.45
ESTROGEN_RESPONSE_EARLY
2236.22
ESTROGEN_RESPONSE_LATE
2202.67
FATTY_ACID_METABOLISM
961.94
G2M_CHECKPOINT
3204.62
GLYCOLYSIS
2255.97
HEDGEHOG_SIGNALING
849.71
HEME_METABOLISM
1619.16
HYPOXIA
3385.11
IL2_STAT5_SIGNALING
2858.23
IL6_JAK_STAT3_SIGNALING
4388.83
INFLAMMATORY_RESPONSE
4965.88
INTERFERON_ALPHA_RESPONSE
943.66
INTERFERON_GAMMA_RESPONSE
5592.82
KRAS_SIGNALING_DN
856.62
KRAS_SIGNALING_UP
3482.66
MITOTIC_SPINDLE
5529.85
MTORC1_SIGNALING
3582.15
MYC_TARGETS_V1
2398.24
MYC_TARGETS_V2
457.22
MYOGENESIS
2582.12
NOTCH_SIGNALING
183.54
OXIDATIVE_PHOSPHORYLATION
1587.23
P53_PATHWAY
2898.79
PANCREAS_BETA_CELLS
108.25
PEROXISOME
871.15
PI3K_AKT_MTOR_SIGNALING
8373.25
PROTEIN_SECRETION
2002.29
REACTIVE_OXYGEN_SPECIES_PATHWAY
460.94
SPERMATOGENESIS
1267.47
TGF_BETA_SIGNALING
1384.57
TNFA_SIGNALING_VIA_NFKB
3490.77
UNFOLDED_PROTEIN_RESPONSE
981.16
UV_RESPONSE_DN
4093.67
UV_RESPONSE_UP
3077.40
WNT_BETA_CATENIN_SIGNALING
1684.74
XENOBIOTIC_METABOLISM
2119.91

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 = 0.823

SampleCancer typecos to ideal
SRR233037520.823
EPT0291EPN0.812
SRR108999840.809
TCGA-FD-A43X-01A-11R-A23W-070.807
aMVAC.P_005_TURBT_S2230.802

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