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 Phase I Trials Completed

Selectivity scorecard

MeasuredDerived
KISS
97.98
Gini
0.702
CATDS
0.027

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 Tenalisib. Strongest target: RET at 98.5% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1RET98.5%1.5%
2TRKC98.1%1.9%
3FGFR398.0%2.0%
4JAK196.4%3.6%
5FGFR296.0%4.0%
6TRKB95.3%4.7%
7JAK293.8%6.2%
8FGFR193.2%6.8%
9ROS_ROS187.4%12.6%
10FGFR483.9%16.1%
11FLT376.8%23.2%
12DDR173.4%26.6%
13TRKA59.0%41.0%
14JAK355.1%44.9%
15LIMK154.4%45.6%
16TYK252.3%47.7%
17MLK3_MAP3K1152.0%48.0%
18FLT4_VEGFR348.7%51.3%
19ALK45.2%54.8%
20C_SRC39.0%61.0%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Tenalisib

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
1528.50
ALLOGRAFT_REJECTION
4353.88
ANDROGEN_RESPONSE
1066.97
ANGIOGENESIS
607.60
APICAL_JUNCTION
4329.63
APICAL_SURFACE
508.09
APOPTOSIS
3100.67
BILE_ACID_METABOLISM
442.95
CHOLESTEROL_HOMEOSTASIS
582.90
COAGULATION
382.96
COMPLEMENT
2297.19
DNA_REPAIR
883.19
E2F_TARGETS
2424.90
EPITHELIAL_MESENCHYMAL_TRANSITION
969.55
ESTROGEN_RESPONSE_EARLY
1426.21
ESTROGEN_RESPONSE_LATE
1612.06
FATTY_ACID_METABOLISM
662.60
G2M_CHECKPOINT
2474.95
GLYCOLYSIS
1482.22
HEDGEHOG_SIGNALING
335.53
HEME_METABOLISM
943.81
HYPOXIA
1952.64
IL2_STAT5_SIGNALING
1666.06
IL6_JAK_STAT3_SIGNALING
4453.47
INFLAMMATORY_RESPONSE
2545.10
INTERFERON_ALPHA_RESPONSE
560.07
INTERFERON_GAMMA_RESPONSE
4130.28
KRAS_SIGNALING_DN
335.77
KRAS_SIGNALING_UP
1551.88
MITOTIC_SPINDLE
2571.15
MTORC1_SIGNALING
1755.14
MYC_TARGETS_V1
1591.81
MYC_TARGETS_V2
359.56
MYOGENESIS
1388.05
NOTCH_SIGNALING
98.07
OXIDATIVE_PHOSPHORYLATION
1161.41
P53_PATHWAY
1423.36
PANCREAS_BETA_CELLS
147.88
PEROXISOME
571.88
PI3K_AKT_MTOR_SIGNALING
5643.91
PROTEIN_SECRETION
1112.30
REACTIVE_OXYGEN_SPECIES_PATHWAY
156.37
SPERMATOGENESIS
890.19
TGF_BETA_SIGNALING
932.70
TNFA_SIGNALING_VIA_NFKB
2470.50
UNFOLDED_PROTEIN_RESPONSE
839.67
UV_RESPONSE_DN
2282.40
UV_RESPONSE_UP
1525.27
WNT_BETA_CATENIN_SIGNALING
948.78
XENOBIOTIC_METABOLISM
886.71

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 = 3.04 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 = 0.834

SampleCancer typecos to ideal
EPT0291EPN0.834
SRR233037520.824
SRR108999840.823
TCGA-FD-A43X-01A-11R-A23W-070.818
TCGA-CF-A5U8-01A-11R-A28M-070.814

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