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
97.47
Gini
0.674
CATDS
0.022

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 Lazertinib. Strongest target: EGFR at 100.0% inhibition.

Accessible data table
RankTargetInhibition %Residual activity %
1EGFR100.0%0.0%
2ERBB2_HER299.7%0.3%
3BLK99.0%1.0%
4ERBB4_HER499.0%1.0%
5JAK397.7%2.3%
6FER97.7%2.3%
7ROS_ROS197.0%3.0%
8TXK97.0%3.0%
9MLK1_MAP3K994.3%5.7%
10MKK793.8%6.2%
11ITK84.0%16.0%
12AXL81.1%18.9%
13MLK3_MAP3K1179.5%20.5%
14BTK77.1%22.9%
15RIPK270.4%29.6%
16TNK168.2%31.8%
17SYK66.4%33.6%
18EPHA663.3%36.7%
19BMX_ETK58.9%41.1%
20RET57.0%43.0%

Selectivity landscape

MeasuredDerived

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

Atlas insights for Lazertinib

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
1285.78
ALLOGRAFT_REJECTION
4394.76
ANDROGEN_RESPONSE
1235.13
ANGIOGENESIS
876.24
APICAL_JUNCTION
4590.86
APICAL_SURFACE
482.07
APOPTOSIS
3084.99
BILE_ACID_METABOLISM
745.86
CHOLESTEROL_HOMEOSTASIS
879.98
COAGULATION
520.06
COMPLEMENT
3173.06
DNA_REPAIR
902.53
E2F_TARGETS
2231.86
EPITHELIAL_MESENCHYMAL_TRANSITION
1012.17
ESTROGEN_RESPONSE_EARLY
1590.32
ESTROGEN_RESPONSE_LATE
1267.96
FATTY_ACID_METABOLISM
276.57
G2M_CHECKPOINT
1980.10
GLYCOLYSIS
1306.04
HEDGEHOG_SIGNALING
653.07
HEME_METABOLISM
919.98
HYPOXIA
1844.17
IL2_STAT5_SIGNALING
1378.24
IL6_JAK_STAT3_SIGNALING
2613.57
INFLAMMATORY_RESPONSE
2927.40
INTERFERON_ALPHA_RESPONSE
362.63
INTERFERON_GAMMA_RESPONSE
3617.66
KRAS_SIGNALING_DN
430.64
KRAS_SIGNALING_UP
1792.51
MITOTIC_SPINDLE
3041.20
MTORC1_SIGNALING
1628.35
MYC_TARGETS_V1
1375.56
MYC_TARGETS_V2
268.11
MYOGENESIS
1401.00
NOTCH_SIGNALING
269.31
OXIDATIVE_PHOSPHORYLATION
620.00
P53_PATHWAY
1480.96
PANCREAS_BETA_CELLS
135.12
PEROXISOME
471.79
PI3K_AKT_MTOR_SIGNALING
4248.71
PROTEIN_SECRETION
1043.18
REACTIVE_OXYGEN_SPECIES_PATHWAY
252.17
SPERMATOGENESIS
752.28
TGF_BETA_SIGNALING
1010.46
TNFA_SIGNALING_VIA_NFKB
2592.26
UNFOLDED_PROTEIN_RESPONSE
782.72
UV_RESPONSE_DN
1996.69
UV_RESPONSE_UP
1882.72
WNT_BETA_CATENIN_SIGNALING
1117.64
XENOBIOTIC_METABOLISM
1065.06

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 = 0.844

SampleCancer typecos to ideal
EPT0291EPN0.844
SRR233037520.843
SRR108999840.835
TCGA-CF-A5U8-01A-11R-A28M-070.831
aMVAC.P_005_TURBT_S2230.830

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