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
0.740
CATDS
0.030

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 Temsirolimus. Strongest target: PDK2_PDHK2 at 36.6% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1PDK2_PDHK236.6%63.4%
2CAMKK232.9%67.1%
3RIPK429.2%70.8%
4PKMYT125.9%74.1%
5WNK125.7%74.3%
6STK21_CIT25.3%74.7%
7ERN1_IRE118.0%82.0%
8MUSK16.4%83.6%
9TRPM7_CHAK116.0%84.0%
10TTBK115.9%84.1%
11OSR1_OXSR115.1%84.9%
12EGFR15.0%85.0%
13MLK3_MAP3K1114.6%85.4%
14STK3314.4%85.6%
15WEE114.1%85.9%
16KHS_MAP4K514.0%86.0%
17PKCD13.8%86.2%
18TTBK213.6%86.4%
19GSK3A13.5%86.5%
20STK39_STLK313.4%86.6%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Temsirolimus

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
247.77
ALLOGRAFT_REJECTION
562.31
ANDROGEN_RESPONSE
322.65
ANGIOGENESIS
104.02
APICAL_JUNCTION
730.10
APICAL_SURFACE
63.43
APOPTOSIS
804.26
BILE_ACID_METABOLISM
113.02
CHOLESTEROL_HOMEOSTASIS
189.76
COAGULATION
70.39
COMPLEMENT
465.00
DNA_REPAIR
255.23
E2F_TARGETS
668.66
EPITHELIAL_MESENCHYMAL_TRANSITION
230.96
ESTROGEN_RESPONSE_EARLY
389.05
ESTROGEN_RESPONSE_LATE
317.92
FATTY_ACID_METABOLISM
86.49
G2M_CHECKPOINT
564.16
GLYCOLYSIS
313.70
HEDGEHOG_SIGNALING
133.54
HEME_METABOLISM
137.19
HYPOXIA
457.38
IL2_STAT5_SIGNALING
319.70
IL6_JAK_STAT3_SIGNALING
410.10
INFLAMMATORY_RESPONSE
414.82
INTERFERON_ALPHA_RESPONSE
77.93
INTERFERON_GAMMA_RESPONSE
502.18
KRAS_SIGNALING_DN
126.38
KRAS_SIGNALING_UP
286.26
MITOTIC_SPINDLE
670.02
MTORC1_SIGNALING
344.57
MYC_TARGETS_V1
421.43
MYC_TARGETS_V2
100.89
MYOGENESIS
352.24
NOTCH_SIGNALING
86.34
OXIDATIVE_PHOSPHORYLATION
106.51
P53_PATHWAY
393.48
PANCREAS_BETA_CELLS
53.72
PEROXISOME
97.53
PI3K_AKT_MTOR_SIGNALING
841.65
PROTEIN_SECRETION
201.87
REACTIVE_OXYGEN_SPECIES_PATHWAY
72.97
SPERMATOGENESIS
203.85
TGF_BETA_SIGNALING
268.59
TNFA_SIGNALING_VIA_NFKB
560.85
UNFOLDED_PROTEIN_RESPONSE
170.83
UV_RESPONSE_DN
389.81
UV_RESPONSE_UP
405.88
WNT_BETA_CATENIN_SIGNALING
368.94
XENOBIOTIC_METABOLISM
162.42

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 = 3.14 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 = 0.881

SampleCancer typecos to ideal
EPT0291EPN0.881
TCGA-CF-A5U8-01A-11R-A28M-070.857
SRR233037520.846
aMVAC.P_005_TURBT_S2230.844
SRR122024980.842

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