{"entity":{"id":"kinase-inhibitors","kind":"technology","name":"Small-molecule kinase inhibitors","aka":[],"tldr":"Pills that block the specific enzyme a cancer relies on. Imatinib in 2001 proved a cancer could be switched off by design.","summary":"Over 80 approved kinase inhibitors: EGFR (osimertinib), ALK (lorlatinib), BRAF/MEK, KRAS G12C, RET, NTRK, MET, FGFR, BTK, JAK, CDK4/6, PI3K/AKT, VEGFR, FLT3, KIT. Resistance through gatekeeper mutations, bypass pathways, and lineage change drives successive generations. Allosteric, covalent, and macrocyclic designs extend the reach.","status":"standard-of-care","asOf":"2026-09-04","wikipedia":"https://en.wikipedia.org/wiki/Tyrosine_kinase_inhibitor","links":[{"label":"Wikipedia","url":"https://en.wikipedia.org/wiki/Tyrosine_kinase_inhibitor"}],"tags":[],"related":["gamma-secretase-inhibitors","hedgehog-inhibitors","her2-tyrosine-kinase-inhibitors","pi3k-akt-mtor-inhibitors"],"cancers":["nsclc"],"sections":["targeted-therapy"],"technologies":[],"targets":["egfr","alk","braf","kras","ret","ntrk","met","fgfr2","kit","flt3","cdk4-6","pik3ca","akt"],"drugs":["fostamatinib","olmutinib"],"companies":["acrivon-therapeutics","alixia","altay-therapeutics","blueprint-medicines","cogent-biosciences","enliven-therapeutics","erasca","fidocure","harmonic-discovery","ideaya-biosciences","nested-therapeutics","oric-pharmaceuticals","prelude-therapeutics","relay-therapeutics","reverie-labs","scorpion-therapeutics","tyra-biosciences","velorum-therapeutics","zentalis-pharmaceuticals","basilea","denovo-biopharma","arog-pharmaceuticals","cyclacel"],"institutions":[],"pathways":[],"terms":["oncogene-addiction","resistance"],"trials":["gefitinib-chemo-tmh"],"people":[],"bottlenecks":[],"keyPapers":["paper-gainor-alk-resistance-mutations-cancer-discov-2016","paper-shaw-alk-resistance-mutations-lorlatinib-jco-2019","paper-oxnard-osimertinib-resistance-mechanisms-jama-oncol-2018"],"journals":[],"dependsOn":[],"notes":["Lung cancer: the generations of inhibitor are also generations of resistance. Each ALK inhibitor selects its own spectrum of kinase-domain mutations, with G1202R dominating after the second generation, and the presence of a mutation is what predicts benefit from the third (69% against 27% response) (Gainor 2016, Shaw 2019). In EGFR-mutant disease the same logic runs T790M to C797S, with the allelic phase of the two deciding whether a combination can cover them (Oxnard 2018)."],"principle":"ATP-competitive or allosteric binding to the kinase domain blocks phosphotransfer.","strengths":["Oral, outpatient","Dramatic responses in oncogene-addicted cancers"],"limitations":["Near-universal resistance in metastatic disease","Off-target toxicities"],"since":2001},"route":"/technologies/kinase-inhibitors/","neighbours":{"technology":[{"id":"drug-resistance-dynamics","kind":"technology","name":"Evolutionary dynamics of drug resistance","route":"/technologies/drug-resistance-dynamics/"},{"id":"gamma-secretase-inhibitors","kind":"technology","name":"Gamma-secretase inhibitors","route":"/technologies/gamma-secretase-inhibitors/"},{"id":"hedgehog-inhibitors","kind":"technology","name":"Hedgehog pathway 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