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
99.49
Gini
0.656
CATDS
0.024

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 Pirtobrutinib. Strongest target: BTK at 97.7% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1BTK97.7%2.3%
2ERBB4_HER495.7%4.3%
3MEK289.3%10.7%
4BRK88.1%11.9%
5YES_YES182.6%17.4%
6MEK181.8%18.2%
7C_KIT69.7%30.3%
8TEC66.9%33.1%
9TXK65.1%34.9%
10JAK263.3%36.7%
11TNIK59.5%40.5%
12LCK58.3%41.7%
13FYN58.1%41.9%
14CSK56.0%44.0%
15FGR53.3%46.7%
16FGFR152.0%48.0%
17IRAK150.1%49.9%
18AURORA_C49.7%50.3%
19FGFR248.9%51.1%
20FMS47.3%52.7%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Pirtobrutinib

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
1499.00
ALLOGRAFT_REJECTION
5638.93
ANDROGEN_RESPONSE
1131.76
ANGIOGENESIS
948.79
APICAL_JUNCTION
5305.97
APICAL_SURFACE
684.99
APOPTOSIS
4062.08
BILE_ACID_METABOLISM
576.30
CHOLESTEROL_HOMEOSTASIS
694.37
COAGULATION
597.50
COMPLEMENT
3051.13
DNA_REPAIR
1230.87
E2F_TARGETS
2809.50
EPITHELIAL_MESENCHYMAL_TRANSITION
1187.97
ESTROGEN_RESPONSE_EARLY
1699.80
ESTROGEN_RESPONSE_LATE
1727.84
FATTY_ACID_METABOLISM
572.20
G2M_CHECKPOINT
2969.57
GLYCOLYSIS
1478.48
HEDGEHOG_SIGNALING
527.13
HEME_METABOLISM
1280.72
HYPOXIA
2534.27
IL2_STAT5_SIGNALING
2047.55
IL6_JAK_STAT3_SIGNALING
3221.94
INFLAMMATORY_RESPONSE
2982.57
INTERFERON_ALPHA_RESPONSE
591.77
INTERFERON_GAMMA_RESPONSE
3753.95
KRAS_SIGNALING_DN
542.64
KRAS_SIGNALING_UP
1952.86
MITOTIC_SPINDLE
3758.14
MTORC1_SIGNALING
2454.79
MYC_TARGETS_V1
1804.46
MYC_TARGETS_V2
387.51
MYOGENESIS
1933.69
NOTCH_SIGNALING
192.51
OXIDATIVE_PHOSPHORYLATION
993.76
P53_PATHWAY
2212.32
PANCREAS_BETA_CELLS
206.38
PEROXISOME
598.14
PI3K_AKT_MTOR_SIGNALING
5497.20
PROTEIN_SECRETION
1292.80
REACTIVE_OXYGEN_SPECIES_PATHWAY
303.21
SPERMATOGENESIS
842.18
TGF_BETA_SIGNALING
1078.63
TNFA_SIGNALING_VIA_NFKB
2678.02
UNFOLDED_PROTEIN_RESPONSE
764.88
UV_RESPONSE_DN
2748.19
UV_RESPONSE_UP
2106.49
WNT_BETA_CATENIN_SIGNALING
1188.16
XENOBIOTIC_METABOLISM
1273.75

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 = 3.10 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 = 0.845

SampleCancer typecos to ideal
EPT0291EPN0.845
SRR233037520.837
TCGA-CF-A5U8-01A-11R-A28M-070.830
SRR108999840.828
TCGA-FD-A43X-01A-11R-A23W-070.826

Annotations

Sign in to read and post annotations.

Loading…