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
93.18
Gini
0.597
CATDS
0.010

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 Neratinib. Strongest target: EGFR at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1EGFR100.0%0.0%
2ERBB4_HER499.7%0.3%
3ERBB2_HER299.7%0.3%
4GLK_MAP4K399.7%0.3%
5LCK99.3%0.7%
6STK25_YSK199.2%0.8%
7KHS_MAP4K599.0%1.0%
8TNIK98.9%1.1%
9MST498.7%1.3%
10MST3_STK2498.3%1.7%
11MINK_MINK198.3%1.7%
12BLK98.2%1.8%
13HGK_MAP4K498.1%1.9%
14C_MER97.8%2.2%
15HPK1_MAP4K197.7%2.4%
16SIK196.4%3.6%
17AXL96.3%3.7%
18ACK195.2%4.8%
19JAK395.2%4.8%
20YES_YES194.3%5.7%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Neratinib

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
3363.92
ALLOGRAFT_REJECTION
10281.37
ANDROGEN_RESPONSE
2559.43
ANGIOGENESIS
1912.07
APICAL_JUNCTION
10610.46
APICAL_SURFACE
1207.99
APOPTOSIS
8484.15
BILE_ACID_METABOLISM
1254.55
CHOLESTEROL_HOMEOSTASIS
1487.09
COAGULATION
1228.69
COMPLEMENT
6300.72
DNA_REPAIR
2449.26
E2F_TARGETS
6666.69
EPITHELIAL_MESENCHYMAL_TRANSITION
3107.01
ESTROGEN_RESPONSE_EARLY
3743.02
ESTROGEN_RESPONSE_LATE
3433.41
FATTY_ACID_METABOLISM
776.54
G2M_CHECKPOINT
6883.18
GLYCOLYSIS
2989.13
HEDGEHOG_SIGNALING
1171.45
HEME_METABOLISM
2520.72
HYPOXIA
5068.07
IL2_STAT5_SIGNALING
3892.12
IL6_JAK_STAT3_SIGNALING
5358.57
INFLAMMATORY_RESPONSE
6297.44
INTERFERON_ALPHA_RESPONSE
1157.08
INTERFERON_GAMMA_RESPONSE
7392.84
KRAS_SIGNALING_DN
1164.51
KRAS_SIGNALING_UP
3974.38
MITOTIC_SPINDLE
8433.22
MTORC1_SIGNALING
4811.23
MYC_TARGETS_V1
4369.56
MYC_TARGETS_V2
1120.21
MYOGENESIS
3836.68
NOTCH_SIGNALING
424.95
OXIDATIVE_PHOSPHORYLATION
1478.90
P53_PATHWAY
5002.62
PANCREAS_BETA_CELLS
498.51
PEROXISOME
1217.78
PI3K_AKT_MTOR_SIGNALING
9836.72
PROTEIN_SECRETION
2089.82
REACTIVE_OXYGEN_SPECIES_PATHWAY
733.72
SPERMATOGENESIS
2198.08
TGF_BETA_SIGNALING
2518.73
TNFA_SIGNALING_VIA_NFKB
5974.27
UNFOLDED_PROTEIN_RESPONSE
1827.82
UV_RESPONSE_DN
5609.67
UV_RESPONSE_UP
4032.62
WNT_BETA_CATENIN_SIGNALING
2712.34
XENOBIOTIC_METABOLISM
2344.91

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 = 3.11 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 = 0.858

SampleCancer typecos to ideal
EPT0291EPN0.858
TCGA-CF-A5U8-01A-11R-A28M-070.849
SRR233037520.842
SRR122024980.838
aMVAC.P_005_TURBT_S2230.834

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