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

Primary targets: AKT1, AKT2, AKT3 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
96.48
Gini
0.644
CATDS
0.013

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 Capivasertib. Strongest target: PKA at 99.7% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1PKA99.7%0.3%
2P70S6K_RPS6KB198.9%1.1%
3AKT398.5%1.5%
4PRKX98.3%1.7%
5PKACB97.8%2.2%
6AKT197.7%2.3%
7LATS296.2%3.8%
8PKG1A96.0%4.0%
9P70S6KB_RPS6KB295.7%4.3%
10AKT295.3%4.7%
11PKCG93.2%6.8%
12MSK2_RPS6KA493.0%7.0%
13MSK1_RPS6KA590.5%9.5%
14PDGFRA90.3%9.7%
15RSK188.8%11.2%
16ROCK188.4%11.6%
17LATS187.7%12.3%
18ROCK285.6%14.4%
19PKCD83.5%16.5%
20PKN3_PRK382.2%17.8%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Capivasertib

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
2589.42
ALLOGRAFT_REJECTION
3595.81
ANDROGEN_RESPONSE
1507.81
ANGIOGENESIS
818.29
APICAL_JUNCTION
5696.81
APICAL_SURFACE
850.99
APOPTOSIS
7188.82
BILE_ACID_METABOLISM
655.74
CHOLESTEROL_HOMEOSTASIS
826.02
COAGULATION
1221.16
COMPLEMENT
3326.91
DNA_REPAIR
1207.69
E2F_TARGETS
5684.24
EPITHELIAL_MESENCHYMAL_TRANSITION
1956.94
ESTROGEN_RESPONSE_EARLY
2638.87
ESTROGEN_RESPONSE_LATE
2398.58
FATTY_ACID_METABOLISM
318.70
G2M_CHECKPOINT
5885.47
GLYCOLYSIS
2387.14
HEDGEHOG_SIGNALING
684.55
HEME_METABOLISM
2899.35
HYPOXIA
4989.54
IL2_STAT5_SIGNALING
2641.39
IL6_JAK_STAT3_SIGNALING
3252.60
INFLAMMATORY_RESPONSE
3567.60
INTERFERON_ALPHA_RESPONSE
624.23
INTERFERON_GAMMA_RESPONSE
3886.71
KRAS_SIGNALING_DN
802.82
KRAS_SIGNALING_UP
1733.90
MITOTIC_SPINDLE
4520.86
MTORC1_SIGNALING
3287.96
MYC_TARGETS_V1
3923.39
MYC_TARGETS_V2
988.79
MYOGENESIS
4079.78
NOTCH_SIGNALING
405.55
OXIDATIVE_PHOSPHORYLATION
1225.94
P53_PATHWAY
3851.31
PANCREAS_BETA_CELLS
746.63
PEROXISOME
854.65
PI3K_AKT_MTOR_SIGNALING
7608.27
PROTEIN_SECRETION
1471.68
REACTIVE_OXYGEN_SPECIES_PATHWAY
184.75
SPERMATOGENESIS
2176.86
TGF_BETA_SIGNALING
2403.68
TNFA_SIGNALING_VIA_NFKB
4893.35
UNFOLDED_PROTEIN_RESPONSE
1589.60
UV_RESPONSE_DN
3588.37
UV_RESPONSE_UP
2831.98
WNT_BETA_CATENIN_SIGNALING
1814.97
XENOBIOTIC_METABOLISM
1439.74

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 = 3.09 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 = 0.853

SampleCancer typecos to ideal
EPT0291EPN0.853
TCGA-CF-A5U8-01A-11R-A28M-070.839
SRR1443713GTEX0.831
R2470.828
SRR122024980.824

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