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

Primary targets: ERBB2_HER2 · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
99.75
Gini
0.652
CATDS
0.054

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 Tucatinib. Strongest target: JAK1 at 92.7% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1JAK192.7%7.3%
2RIPK436.0%64.0%
3JAK233.6%66.4%
4TYK229.5%70.5%
5AURORA_A28.4%71.6%
6STK38_NDR120.5%79.5%
7COT1_MAP3K818.9%81.1%
8CDK1_CYCLIN_E17.7%82.3%
9MEKK617.6%82.4%
10PKCIOTA17.3%82.7%
11WNK317.2%82.8%
12TRKB16.4%83.6%
13CDK4_CYCLIN_D116.4%83.6%
14CDK4_CYCLIN_D315.6%84.4%
15LRRK215.0%85.0%
16TAOK3_JIK14.8%85.2%
17FAK_PTK214.6%85.4%
18CDK1_CYCLIN_B14.3%85.7%
19CAMK414.1%85.9%
20AURORA_B13.7%86.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Tucatinib

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
664.16
ALLOGRAFT_REJECTION
1655.75
ANDROGEN_RESPONSE
282.49
ANGIOGENESIS
157.30
APICAL_JUNCTION
1328.70
APICAL_SURFACE
226.76
APOPTOSIS
1353.80
BILE_ACID_METABOLISM
131.97
CHOLESTEROL_HOMEOSTASIS
131.40
COAGULATION
137.52
COMPLEMENT
867.13
DNA_REPAIR
317.71
E2F_TARGETS
1107.69
EPITHELIAL_MESENCHYMAL_TRANSITION
369.72
ESTROGEN_RESPONSE_EARLY
752.95
ESTROGEN_RESPONSE_LATE
682.10
FATTY_ACID_METABOLISM
119.03
G2M_CHECKPOINT
1080.11
GLYCOLYSIS
460.30
HEDGEHOG_SIGNALING
80.74
HEME_METABOLISM
500.33
HYPOXIA
770.76
IL2_STAT5_SIGNALING
975.34
IL6_JAK_STAT3_SIGNALING
1857.53
INFLAMMATORY_RESPONSE
1429.49
INTERFERON_ALPHA_RESPONSE
340.98
INTERFERON_GAMMA_RESPONSE
1862.29
KRAS_SIGNALING_DN
185.12
KRAS_SIGNALING_UP
650.38
MITOTIC_SPINDLE
955.95
MTORC1_SIGNALING
628.03
MYC_TARGETS_V1
741.47
MYC_TARGETS_V2
185.54
MYOGENESIS
709.02
NOTCH_SIGNALING
70.40
OXIDATIVE_PHOSPHORYLATION
177.46
P53_PATHWAY
776.27
PANCREAS_BETA_CELLS
80.33
PEROXISOME
180.18
PI3K_AKT_MTOR_SIGNALING
1738.77
PROTEIN_SECRETION
335.65
REACTIVE_OXYGEN_SPECIES_PATHWAY
91.04
SPERMATOGENESIS
433.32
TGF_BETA_SIGNALING
366.95
TNFA_SIGNALING_VIA_NFKB
1238.69
UNFOLDED_PROTEIN_RESPONSE
414.10
UV_RESPONSE_DN
922.16
UV_RESPONSE_UP
719.42
WNT_BETA_CATENIN_SIGNALING
468.28
XENOBIOTIC_METABOLISM
230.78

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 = 2.96 bits (max possible across 10 hallmarks = 3.32 bits). Moderately broad.

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 = 0.853

SampleCancer typecos to ideal
EPT0291EPN0.853
TCGA-CF-A5U8-01A-11R-A28M-070.840
TCGA-CV-7424-01A-11R-2081-070.838
SRR108999840.838
C3L-037260.835

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