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

Primary targets: JAK1, JAK2, JAK3, TYK2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
98.25
Gini
0.592
CATDS
0.018

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 Ruxolitinib. Strongest target: JAK2 at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1JAK2100.0%0.0%
2JAK399.2%0.8%
3TYK299.0%1.0%
4JAK196.7%3.3%
5CAMK2A93.0%7.0%
6CAMK2D90.5%9.5%
7STK38L_NDR290.0%10.0%
8DMPK287.1%12.9%
9STK38_NDR186.6%13.4%
10ACK178.5%21.5%
11TRKC75.2%24.8%
12LATS171.2%28.8%
13CDK8_CYCLIN_C69.0%31.0%
14CDK19_CYCLIN_C66.6%33.4%
15ROCK163.6%36.4%
16LRRK263.0%37.0%
17MEKK357.0%43.0%
18LIMK154.3%45.7%
19MEKK252.6%47.4%
20ALK52.1%47.9%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Ruxolitinib

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
1944.94
ALLOGRAFT_REJECTION
4629.13
ANDROGEN_RESPONSE
1570.16
ANGIOGENESIS
697.62
APICAL_JUNCTION
4594.60
APICAL_SURFACE
601.98
APOPTOSIS
5032.48
BILE_ACID_METABOLISM
552.15
CHOLESTEROL_HOMEOSTASIS
671.04
COAGULATION
457.31
COMPLEMENT
2884.21
DNA_REPAIR
1082.61
E2F_TARGETS
3759.85
EPITHELIAL_MESENCHYMAL_TRANSITION
2077.49
ESTROGEN_RESPONSE_EARLY
2927.63
ESTROGEN_RESPONSE_LATE
2697.87
FATTY_ACID_METABOLISM
336.62
G2M_CHECKPOINT
3818.71
GLYCOLYSIS
2102.98
HEDGEHOG_SIGNALING
624.96
HEME_METABOLISM
1489.43
HYPOXIA
2851.16
IL2_STAT5_SIGNALING
2072.35
IL6_JAK_STAT3_SIGNALING
4193.79
INFLAMMATORY_RESPONSE
3516.34
INTERFERON_ALPHA_RESPONSE
679.49
INTERFERON_GAMMA_RESPONSE
4511.69
KRAS_SIGNALING_DN
966.58
KRAS_SIGNALING_UP
1687.23
MITOTIC_SPINDLE
3769.15
MTORC1_SIGNALING
2202.99
MYC_TARGETS_V1
2263.98
MYC_TARGETS_V2
569.98
MYOGENESIS
3147.62
NOTCH_SIGNALING
210.84
OXIDATIVE_PHOSPHORYLATION
564.52
P53_PATHWAY
2390.09
PANCREAS_BETA_CELLS
238.45
PEROXISOME
881.45
PI3K_AKT_MTOR_SIGNALING
5937.58
PROTEIN_SECRETION
1707.31
REACTIVE_OXYGEN_SPECIES_PATHWAY
212.33
SPERMATOGENESIS
1338.19
TGF_BETA_SIGNALING
1554.07
TNFA_SIGNALING_VIA_NFKB
3678.35
UNFOLDED_PROTEIN_RESPONSE
1336.48
UV_RESPONSE_DN
3172.86
UV_RESPONSE_UP
2662.98
WNT_BETA_CATENIN_SIGNALING
1625.10
XENOBIOTIC_METABOLISM
1076.93

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 = 0.865

SampleCancer typecos to ideal
EPT0291EPN0.865
TCGA-CF-A5U8-01A-11R-A28M-070.853
SRR233037520.845
aMVAC.P_005_TURBT_S2230.838
SRR122024980.837

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