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

Primary targets: TYK2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
98.99
Gini
0.718
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 Deucravacitinib. Strongest target: C_MET at 97.9% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1C_MET97.9%2.1%
2FGFR393.3%6.7%
3FGFR292.5%7.5%
4FGFR492.0%8.0%
5FGFR185.1%14.9%
6EIF2AK283.2%16.8%
7GSK3B75.0%25.0%
8FLT4_VEGFR366.8%33.2%
9HPK1_MAP4K164.0%36.0%
10FLT1_VEGFR161.9%38.1%
11BMPR260.8%39.2%
12LCK56.7%43.3%
13LYN49.8%50.2%
14TNIK49.1%50.9%
15FMS46.0%54.0%
16RET45.5%54.5%
17C_KIT45.4%54.6%
18DDR144.8%55.2%
19TYRO3_SKY42.0%58.0%
20ABL139.7%60.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Deucravacitinib

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-target1%
Off-target99%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
1979.91
ALLOGRAFT_REJECTION
4683.79
ANDROGEN_RESPONSE
1576.79
ANGIOGENESIS
734.46
APICAL_JUNCTION
5012.52
APICAL_SURFACE
508.63
APOPTOSIS
5213.49
BILE_ACID_METABOLISM
398.49
CHOLESTEROL_HOMEOSTASIS
754.78
COAGULATION
548.07
COMPLEMENT
2661.22
DNA_REPAIR
1723.69
E2F_TARGETS
4030.63
EPITHELIAL_MESENCHYMAL_TRANSITION
1471.82
ESTROGEN_RESPONSE_EARLY
2287.36
ESTROGEN_RESPONSE_LATE
2440.88
FATTY_ACID_METABOLISM
526.63
G2M_CHECKPOINT
4626.88
GLYCOLYSIS
1878.63
HEDGEHOG_SIGNALING
494.50
HEME_METABOLISM
1902.00
HYPOXIA
2955.11
IL2_STAT5_SIGNALING
2293.78
IL6_JAK_STAT3_SIGNALING
3316.43
INFLAMMATORY_RESPONSE
2688.86
INTERFERON_ALPHA_RESPONSE
571.12
INTERFERON_GAMMA_RESPONSE
4121.87
KRAS_SIGNALING_DN
608.18
KRAS_SIGNALING_UP
1987.70
MITOTIC_SPINDLE
4381.39
MTORC1_SIGNALING
2574.21
MYC_TARGETS_V1
2984.89
MYC_TARGETS_V2
711.92
MYOGENESIS
2194.46
NOTCH_SIGNALING
265.11
OXIDATIVE_PHOSPHORYLATION
945.90
P53_PATHWAY
3075.42
PANCREAS_BETA_CELLS
498.99
PEROXISOME
967.62
PI3K_AKT_MTOR_SIGNALING
5959.27
PROTEIN_SECRETION
1240.64
REACTIVE_OXYGEN_SPECIES_PATHWAY
492.51
SPERMATOGENESIS
1103.60
TGF_BETA_SIGNALING
1849.73
TNFA_SIGNALING_VIA_NFKB
3629.28
UNFOLDED_PROTEIN_RESPONSE
1018.58
UV_RESPONSE_DN
3500.10
UV_RESPONSE_UP
2216.59
WNT_BETA_CATENIN_SIGNALING
1407.85
XENOBIOTIC_METABOLISM
1245.63

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 = 0.865

SampleCancer typecos to ideal
EPT0291EPN0.865
TCGA-CF-A5U8-01A-11R-A28M-070.845
SRR122024980.843
SRR233037520.841
aMVAC.P_005_TURBT_S2230.839

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