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

Primary targets: EGFR · FDA status: FDA Approved

Selectivity scorecard

MeasuredDerived
KISS
99.75
Gini
0.695
CATDS
0.027

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 Erlotinib. Strongest target: EGFR at 99.4% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1EGFR99.4%0.6%
2LOK_STK1089.5%10.5%
3DDR183.5%16.5%
4ERBB4_HER477.6%22.4%
5ERBB2_HER277.5%22.5%
6MEK570.9%29.1%
7ABL170.5%29.5%
8SLK_STK268.6%31.4%
9ABL2_ARG66.8%33.2%
10FLT361.3%38.7%
11LYN59.6%40.4%
12DDR251.2%48.8%
13FGFR250.7%49.3%
14EPHA650.0%50.0%
15LCK49.7%50.3%
16RET49.5%50.5%
17FLT4_VEGFR348.7%51.3%
18BLK48.0%52.0%
19MNK147.6%52.4%
20RIPK244.7%55.3%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Erlotinib

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-target23%
Off-target77%
Ghost (2nd-order)0%
PathwayCompositionTotal |Π|
ADIPOGENESIS
1611.54
ALLOGRAFT_REJECTION
4788.67
ANDROGEN_RESPONSE
1066.98
ANGIOGENESIS
917.28
APICAL_JUNCTION
5191.80
APICAL_SURFACE
619.01
APOPTOSIS
4072.42
BILE_ACID_METABOLISM
608.25
CHOLESTEROL_HOMEOSTASIS
1194.48
COAGULATION
590.95
COMPLEMENT
3291.76
DNA_REPAIR
1222.00
E2F_TARGETS
2637.31
EPITHELIAL_MESENCHYMAL_TRANSITION
1051.68
ESTROGEN_RESPONSE_EARLY
1628.83
ESTROGEN_RESPONSE_LATE
1639.94
FATTY_ACID_METABOLISM
472.86
G2M_CHECKPOINT
2221.20
GLYCOLYSIS
1555.43
HEDGEHOG_SIGNALING
524.57
HEME_METABOLISM
1132.27
HYPOXIA
2495.27
IL2_STAT5_SIGNALING
1760.90
IL6_JAK_STAT3_SIGNALING
2961.22
INFLAMMATORY_RESPONSE
2908.61
INTERFERON_ALPHA_RESPONSE
552.46
INTERFERON_GAMMA_RESPONSE
3648.11
KRAS_SIGNALING_DN
541.14
KRAS_SIGNALING_UP
2158.99
MITOTIC_SPINDLE
3866.78
MTORC1_SIGNALING
2161.48
MYC_TARGETS_V1
1972.43
MYC_TARGETS_V2
377.60
MYOGENESIS
1589.58
NOTCH_SIGNALING
215.24
OXIDATIVE_PHOSPHORYLATION
927.68
P53_PATHWAY
2226.60
PANCREAS_BETA_CELLS
172.43
PEROXISOME
763.22
PI3K_AKT_MTOR_SIGNALING
4893.14
PROTEIN_SECRETION
1266.35
REACTIVE_OXYGEN_SPECIES_PATHWAY
361.24
SPERMATOGENESIS
761.26
TGF_BETA_SIGNALING
1090.89
TNFA_SIGNALING_VIA_NFKB
2450.70
UNFOLDED_PROTEIN_RESPONSE
717.38
UV_RESPONSE_DN
2521.69
UV_RESPONSE_UP
2184.21
WNT_BETA_CATENIN_SIGNALING
1240.87
XENOBIOTIC_METABOLISM
1219.56

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 = 0.850

SampleCancer typecos to ideal
EPT0291EPN0.850
SRR233037520.848
aMVAC.P_005_TURBT_S2230.833
SRR108999840.833
SRR122024980.830

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