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

Primary targets: FKBP12, MTOR_FRAP1 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
100.00
Gini
0.706
CATDS
0.024

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 Everolimus. Strongest target: PKMYT1 at 33.8% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1PKMYT133.8%66.2%
2CAMKK228.8%71.2%
3PDK2_PDHK228.6%71.4%
4ERN1_IRE125.3%74.7%
5STK3322.2%77.8%
6ALK2_ACVR121.6%78.4%
7GSK3A21.5%78.5%
8MLK3_MAP3K1121.1%78.9%
9MUSK19.4%80.6%
10EGFR17.8%82.2%
11WEE117.6%82.4%
12CK1D17.5%82.5%
13TRPM7_CHAK116.7%83.3%
14CTK_MATK16.4%83.6%
15NEK816.4%83.6%
16ABL116.0%84.0%
17TESK115.8%84.2%
18TTBK215.6%84.4%
19ROS_ROS115.6%84.4%
20PHKG115.6%84.4%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Everolimus

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
328.16
ALLOGRAFT_REJECTION
674.90
ANDROGEN_RESPONSE
306.52
ANGIOGENESIS
109.48
APICAL_JUNCTION
797.97
APICAL_SURFACE
110.76
APOPTOSIS
994.03
BILE_ACID_METABOLISM
103.80
CHOLESTEROL_HOMEOSTASIS
276.72
COAGULATION
103.51
COMPLEMENT
516.36
DNA_REPAIR
310.36
E2F_TARGETS
858.16
EPITHELIAL_MESENCHYMAL_TRANSITION
281.52
ESTROGEN_RESPONSE_EARLY
467.18
ESTROGEN_RESPONSE_LATE
329.40
FATTY_ACID_METABOLISM
88.62
G2M_CHECKPOINT
675.22
GLYCOLYSIS
363.30
HEDGEHOG_SIGNALING
103.01
HEME_METABOLISM
197.44
HYPOXIA
651.72
IL2_STAT5_SIGNALING
428.95
IL6_JAK_STAT3_SIGNALING
569.05
INFLAMMATORY_RESPONSE
548.41
INTERFERON_ALPHA_RESPONSE
107.63
INTERFERON_GAMMA_RESPONSE
675.11
KRAS_SIGNALING_DN
140.41
KRAS_SIGNALING_UP
341.81
MITOTIC_SPINDLE
821.53
MTORC1_SIGNALING
390.20
MYC_TARGETS_V1
531.62
MYC_TARGETS_V2
177.67
MYOGENESIS
443.79
NOTCH_SIGNALING
89.42
OXIDATIVE_PHOSPHORYLATION
110.19
P53_PATHWAY
606.66
PANCREAS_BETA_CELLS
63.79
PEROXISOME
137.12
PI3K_AKT_MTOR_SIGNALING
1042.91
PROTEIN_SECRETION
194.73
REACTIVE_OXYGEN_SPECIES_PATHWAY
64.49
SPERMATOGENESIS
248.33
TGF_BETA_SIGNALING
328.78
TNFA_SIGNALING_VIA_NFKB
669.44
UNFOLDED_PROTEIN_RESPONSE
173.11
UV_RESPONSE_DN
532.11
UV_RESPONSE_UP
449.64
WNT_BETA_CATENIN_SIGNALING
397.10
XENOBIOTIC_METABOLISM
204.02

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 = 3.12 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 = 0.880

SampleCancer typecos to ideal
EPT0291EPN0.880
TCGA-CF-A5U8-01A-11R-A28M-070.856
SRR1443713GTEX0.849
SRR122024980.841
aMVAC.P_005_TURBT_S2230.840

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