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

Primary targets: PI3K, MTOR_FRAP1 · FDA status: Phase III FDA Trials

Selectivity scorecard

MeasuredDerived
KISS
99.75
Gini
0.611
CATDS
0.044

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 Gedatolisib. Strongest target: MTOR_FRAP1 at 95.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1MTOR_FRAP195.0%5.0%
2DNA_PK73.5%26.5%
3BRAF56.5%43.5%
4TAOK2_TAO148.6%51.4%
5RAF134.9%65.1%
6ARAF31.9%68.1%
7EIF2AK223.8%76.2%
8CK1EPSILON21.0%79.0%
9MYO3B20.3%79.7%
10NEK919.0%81.0%
11CK1G118.1%81.9%
12LOK_STK1018.0%82.0%
13PKCB117.6%82.4%
14SNRK17.0%83.0%
15CDK9_CYCLIN_T216.4%83.6%
16RIPK516.3%83.7%
17SLK_STK215.6%84.4%
18LATS215.6%84.4%
19TAOK115.5%84.5%
20DMPK215.4%84.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Gedatolisib

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
575.05
ALLOGRAFT_REJECTION
1140.69
ANDROGEN_RESPONSE
512.53
ANGIOGENESIS
212.60
APICAL_JUNCTION
1389.95
APICAL_SURFACE
158.13
APOPTOSIS
1410.09
BILE_ACID_METABOLISM
158.49
CHOLESTEROL_HOMEOSTASIS
148.24
COAGULATION
144.97
COMPLEMENT
833.45
DNA_REPAIR
477.55
E2F_TARGETS
1499.64
EPITHELIAL_MESENCHYMAL_TRANSITION
542.33
ESTROGEN_RESPONSE_EARLY
847.20
ESTROGEN_RESPONSE_LATE
720.27
FATTY_ACID_METABOLISM
84.17
G2M_CHECKPOINT
1489.96
GLYCOLYSIS
566.84
HEDGEHOG_SIGNALING
211.11
HEME_METABOLISM
586.45
HYPOXIA
785.48
IL2_STAT5_SIGNALING
662.46
IL6_JAK_STAT3_SIGNALING
815.74
INFLAMMATORY_RESPONSE
1090.02
INTERFERON_ALPHA_RESPONSE
205.26
INTERFERON_GAMMA_RESPONSE
1164.00
KRAS_SIGNALING_DN
326.32
KRAS_SIGNALING_UP
513.65
MITOTIC_SPINDLE
1333.07
MTORC1_SIGNALING
860.72
MYC_TARGETS_V1
971.99
MYC_TARGETS_V2
276.39
MYOGENESIS
768.19
NOTCH_SIGNALING
86.79
OXIDATIVE_PHOSPHORYLATION
161.51
P53_PATHWAY
872.84
PANCREAS_BETA_CELLS
143.36
PEROXISOME
252.20
PI3K_AKT_MTOR_SIGNALING
1803.30
PROTEIN_SECRETION
442.49
REACTIVE_OXYGEN_SPECIES_PATHWAY
105.95
SPERMATOGENESIS
551.96
TGF_BETA_SIGNALING
454.63
TNFA_SIGNALING_VIA_NFKB
1284.31
UNFOLDED_PROTEIN_RESPONSE
390.11
UV_RESPONSE_DN
1035.63
UV_RESPONSE_UP
705.66
WNT_BETA_CATENIN_SIGNALING
519.15
XENOBIOTIC_METABOLISM
331.94

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 = 0.869

SampleCancer typecos to ideal
EPT0291EPN0.869
TCGA-CF-A5U8-01A-11R-A28M-070.865
SRR122024980.840
SRR1443713GTEX0.839
SRR233037520.834

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