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

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

Selectivity scorecard

MeasuredDerived
KISS
97.99
Gini
0.616
CATDS
0.014

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 Baricitinib. Strongest target: STK38L_NDR2 at 99.4% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1STK38L_NDR299.4%0.6%
2JAK198.1%1.9%
3TYK297.3%2.7%
4JAK297.2%2.8%
5STK38_NDR197.1%2.9%
6JAK397.0%3.0%
7STK22D_TSSK191.7%8.3%
8PKA90.9%9.1%
9PKCG88.2%11.8%
10LATS186.4%13.6%
11CAMK2D82.2%17.8%
12DAPK181.9%18.1%
13ROCK181.7%18.3%
14DMPK281.2%18.9%
15PKACB80.3%19.7%
16PKACG79.9%20.1%
17ACK179.5%20.5%
18PKCD76.9%23.1%
19ROCK276.5%23.5%
20P70S6K_RPS6KB174.7%25.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Baricitinib

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
2272.34
ALLOGRAFT_REJECTION
5309.79
ANDROGEN_RESPONSE
1825.95
ANGIOGENESIS
792.75
APICAL_JUNCTION
5440.49
APICAL_SURFACE
645.50
APOPTOSIS
5695.83
BILE_ACID_METABOLISM
634.07
CHOLESTEROL_HOMEOSTASIS
585.31
COAGULATION
616.41
COMPLEMENT
3136.11
DNA_REPAIR
1314.42
E2F_TARGETS
4436.81
EPITHELIAL_MESENCHYMAL_TRANSITION
2205.83
ESTROGEN_RESPONSE_EARLY
2867.54
ESTROGEN_RESPONSE_LATE
2858.56
FATTY_ACID_METABOLISM
369.11
G2M_CHECKPOINT
4515.96
GLYCOLYSIS
2202.39
HEDGEHOG_SIGNALING
673.76
HEME_METABOLISM
2005.66
HYPOXIA
2991.30
IL2_STAT5_SIGNALING
2364.26
IL6_JAK_STAT3_SIGNALING
4488.10
INFLAMMATORY_RESPONSE
3900.38
INTERFERON_ALPHA_RESPONSE
735.11
INTERFERON_GAMMA_RESPONSE
5174.12
KRAS_SIGNALING_DN
912.49
KRAS_SIGNALING_UP
2198.07
MITOTIC_SPINDLE
4141.80
MTORC1_SIGNALING
2634.30
MYC_TARGETS_V1
2647.62
MYC_TARGETS_V2
662.81
MYOGENESIS
3351.43
NOTCH_SIGNALING
250.34
OXIDATIVE_PHOSPHORYLATION
613.04
P53_PATHWAY
2633.40
PANCREAS_BETA_CELLS
365.73
PEROXISOME
934.60
PI3K_AKT_MTOR_SIGNALING
6758.18
PROTEIN_SECRETION
1759.45
REACTIVE_OXYGEN_SPECIES_PATHWAY
212.00
SPERMATOGENESIS
1607.40
TGF_BETA_SIGNALING
1718.04
TNFA_SIGNALING_VIA_NFKB
4097.75
UNFOLDED_PROTEIN_RESPONSE
1401.78
UV_RESPONSE_DN
3387.28
UV_RESPONSE_UP
2766.44
WNT_BETA_CATENIN_SIGNALING
1651.57
XENOBIOTIC_METABOLISM
1221.07

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 = 0.861

SampleCancer typecos to ideal
EPT0291EPN0.861
TCGA-CF-A5U8-01A-11R-A28M-070.855
SRR233037520.842
SRR122024980.837
TCGA-FD-A43X-01A-11R-A23W-070.837

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