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

Primary targets: PI3K · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
100.00
Gini
0.604
CATDS
0.017

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 Leniolisib. Strongest target: AKT3 at 27.4% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1AKT327.4%72.6%
2DAPK220.1%79.9%
3SYK19.5%80.5%
4STK3319.2%80.8%
5ALK4_ACVR1B18.6%81.4%
6MAST318.0%82.0%
7MEKK317.2%82.8%
8WNK317.0%83.0%
9CDC7_DBF415.8%84.2%
10ERK115.8%84.2%
11CDK1_CYCLIN_A15.7%84.3%
12PDK3_PDHK315.7%84.3%
13DNA_PK15.6%84.4%
14EPHA615.3%84.7%
15TYRO3_SKY15.2%84.8%
16RAF115.2%84.8%
17CDK6_CYCLIN_D314.3%85.7%
18JNK213.5%86.5%
19ERN1_IRE113.4%86.6%
20PKG1B13.4%86.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Leniolisib

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
418.57
ALLOGRAFT_REJECTION
921.08
ANDROGEN_RESPONSE
386.74
ANGIOGENESIS
123.26
APICAL_JUNCTION
1098.71
APICAL_SURFACE
154.03
APOPTOSIS
1311.72
BILE_ACID_METABOLISM
141.60
CHOLESTEROL_HOMEOSTASIS
130.73
COAGULATION
171.81
COMPLEMENT
647.69
DNA_REPAIR
266.95
E2F_TARGETS
1194.23
EPITHELIAL_MESENCHYMAL_TRANSITION
411.46
ESTROGEN_RESPONSE_EARLY
684.40
ESTROGEN_RESPONSE_LATE
572.22
FATTY_ACID_METABOLISM
94.57
G2M_CHECKPOINT
1039.45
GLYCOLYSIS
526.28
HEDGEHOG_SIGNALING
94.89
HEME_METABOLISM
460.58
HYPOXIA
806.25
IL2_STAT5_SIGNALING
464.42
IL6_JAK_STAT3_SIGNALING
651.39
INFLAMMATORY_RESPONSE
788.75
INTERFERON_ALPHA_RESPONSE
146.51
INTERFERON_GAMMA_RESPONSE
831.57
KRAS_SIGNALING_DN
228.81
KRAS_SIGNALING_UP
390.19
MITOTIC_SPINDLE
958.49
MTORC1_SIGNALING
688.23
MYC_TARGETS_V1
773.64
MYC_TARGETS_V2
252.18
MYOGENESIS
655.83
NOTCH_SIGNALING
96.02
OXIDATIVE_PHOSPHORYLATION
188.92
P53_PATHWAY
712.95
PANCREAS_BETA_CELLS
106.00
PEROXISOME
178.46
PI3K_AKT_MTOR_SIGNALING
1468.65
PROTEIN_SECRETION
258.86
REACTIVE_OXYGEN_SPECIES_PATHWAY
65.07
SPERMATOGENESIS
460.64
TGF_BETA_SIGNALING
381.55
TNFA_SIGNALING_VIA_NFKB
933.94
UNFOLDED_PROTEIN_RESPONSE
346.37
UV_RESPONSE_DN
738.21
UV_RESPONSE_UP
560.15
WNT_BETA_CATENIN_SIGNALING
425.91
XENOBIOTIC_METABOLISM
316.67

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 = 0.868

SampleCancer typecos to ideal
EPT0291EPN0.868
TCGA-CF-A5U8-01A-11R-A28M-070.851
SRR1443713GTEX0.834
SRR122024980.833
R2470.833

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