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
0.679
CATDS
0.022

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 Inavolisib. Strongest target: DNA_PK at 24.2% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1DNA_PK24.2%75.8%
2LRRK221.6%78.4%
3WNK320.9%79.1%
4IKKE_IKBKE17.9%82.1%
5SGK216.2%83.8%
6ERK114.3%85.7%
7PLK313.2%86.8%
8PAK512.2%87.8%
9MLK3_MAP3K1112.1%87.9%
10CDK9_CYCLIN_K12.0%88.0%
11RIPK412.0%88.0%
12P38G11.7%88.3%
13MST411.6%88.4%
14P38D_MAPK1311.6%88.4%
15PDK2_PDHK211.5%88.5%
16ALK2_ACVR111.1%88.9%
17ERK5_MAPK710.7%89.3%
18CAMK1A10.7%89.3%
19CAMKK110.4%89.6%
20CDK4_CYCLIN_D310.4%89.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Inavolisib

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
167.04
ALLOGRAFT_REJECTION
556.30
ANDROGEN_RESPONSE
172.46
ANGIOGENESIS
120.67
APICAL_JUNCTION
580.50
APICAL_SURFACE
107.01
APOPTOSIS
651.99
BILE_ACID_METABOLISM
57.83
CHOLESTEROL_HOMEOSTASIS
82.82
COAGULATION
104.98
COMPLEMENT
340.32
DNA_REPAIR
146.07
E2F_TARGETS
462.55
EPITHELIAL_MESENCHYMAL_TRANSITION
143.86
ESTROGEN_RESPONSE_EARLY
300.13
ESTROGEN_RESPONSE_LATE
271.52
FATTY_ACID_METABOLISM
36.23
G2M_CHECKPOINT
427.60
GLYCOLYSIS
188.10
HEDGEHOG_SIGNALING
47.45
HEME_METABOLISM
217.37
HYPOXIA
418.26
IL2_STAT5_SIGNALING
266.22
IL6_JAK_STAT3_SIGNALING
266.72
INFLAMMATORY_RESPONSE
346.78
INTERFERON_ALPHA_RESPONSE
60.85
INTERFERON_GAMMA_RESPONSE
380.12
KRAS_SIGNALING_DN
113.49
KRAS_SIGNALING_UP
154.18
MITOTIC_SPINDLE
477.04
MTORC1_SIGNALING
333.40
MYC_TARGETS_V1
331.19
MYC_TARGETS_V2
103.23
MYOGENESIS
274.38
NOTCH_SIGNALING
17.07
OXIDATIVE_PHOSPHORYLATION
93.02
P53_PATHWAY
407.65
PANCREAS_BETA_CELLS
47.90
PEROXISOME
90.10
PI3K_AKT_MTOR_SIGNALING
692.47
PROTEIN_SECRETION
170.14
REACTIVE_OXYGEN_SPECIES_PATHWAY
37.59
SPERMATOGENESIS
119.93
TGF_BETA_SIGNALING
133.12
TNFA_SIGNALING_VIA_NFKB
313.13
UNFOLDED_PROTEIN_RESPONSE
152.90
UV_RESPONSE_DN
317.61
UV_RESPONSE_UP
305.41
WNT_BETA_CATENIN_SIGNALING
181.38
XENOBIOTIC_METABOLISM
150.86

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 = 0.858

SampleCancer typecos to ideal
EPT0291EPN0.858
TCGA-CF-A5U8-01A-11R-A28M-070.832
SRR233037520.831
C3N-034200.827
SRR122024980.826

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