{"entity":{"id":"hma","kind":"term","name":"Hypomethylating agents (azacitidine, decitabine)","aka":["HMA","HMAs","hypomethylating","hypomethylating agent","hypomethylating agents","oral azacitidine","oral decitabine-cedazuridine","venetoclax-azacitidine","venetoclax + azacitidine","ven-aza","Ven/Aza","HMA-venetoclax","venetoclax + HMA","HMA failure"],"tldr":"Low-intensity chemotherapy that strips chemical 'off' switches (methyl groups) from DNA so silenced genes can be read again. The mainstay for older patients with AML and high-risk MDS, especially combined with venetoclax.","summary":"Azacitidine and decitabine (approved 2004-06) extend survival in higher-risk MDS and were the only option for AML patients unfit for intensive chemotherapy until venetoclax-azacitidine (VIALE-A, 2020) roughly doubled responses and became the standard, now available fully orally. They are given in outpatient cycles for as long as they work; 'HMA failure' defines a population with very poor outcomes where menin inhibitors, IDH inhibitors and trials of new agents are focused. Response can take several cycles, so early stopping is a common error.","asOf":"2026-09-09","wikipedia":"https://en.wikipedia.org/wiki/Azacitidine","links":[{"label":"Wikipedia","url":"https://en.wikipedia.org/wiki/Azacitidine"}],"tags":[],"related":["mds","seven-plus-three","performance-status"],"cancers":["aml"],"sections":["epigenetics","chemotherapy"],"technologies":["epigenetic-drugs"],"targets":[],"drugs":["azacitidine","venetoclax"],"companies":[],"institutions":[],"pathways":[],"terms":[],"trials":[],"people":[],"bottlenecks":[],"keyPapers":[],"journals":[],"dependsOn":[],"notes":[],"category":"Treatment jargon"},"route":"/terms/hma/","neighbours":{"cancer":[{"id":"aml","kind":"cancer","name":"Acute myeloid leukaemia","route":"/cancers/aml/"},{"id":"aml-older-unfit","kind":"cancer","name":"Acute myeloid leukaemia in older or unfit patients","route":"/cancers/aml-older-unfit/"},{"id":"cmml","kind":"cancer","name":"Chronic myelomonocytic leukaemia and MDS/MPN overlap neoplasms","route":"/cancers/cmml/"},{"id":"mds-higher-risk","kind":"cancer","name":"Higher-risk myelodysplastic syndromes","route":"/cancers/mds-higher-risk/"},{"id":"aml-idh","kind":"cancer","name":"IDH1- and IDH2-mutated acute myeloid leukaemia","route":"/cancers/aml-idh/"},{"id":"mds","kind":"cancer","name":"Myelodysplastic syndromes / neoplasms (MDS)","route":"/cancers/mds/"},{"id":"aml-secondary","kind":"cancer","name":"Secondary and therapy-related acute myeloid leukaemia","route":"/cancers/aml-secondary/"}],"term":[{"id":"seven-plus-three","kind":"term","name":"7+3 induction chemotherapy","route":"/terms/seven-plus-three/"},{"id":"ipss-m-ipss-r","kind":"term","name":"IPSS-R and IPSS-M (myelodysplastic syndrome risk scores)","route":"/terms/ipss-m-ipss-r/"},{"id":"performance-status","kind":"term","name":"Performance status (ECOG, Karnofsky)","route":"/terms/performance-status/"}],"section":[{"id":"chemotherapy","kind":"section","name":"Chemotherapy","route":"/fronts/chemotherapy/"},{"id":"epigenetics","kind":"section","name":"Epigenetic & Transcriptional Therapy","route":"/fronts/epigenetics/"}],"technology":[{"id":"epigenetic-drugs","kind":"technology","name":"Epigenetic drugs (HDAC, DNMT, EZH2, IDH, menin, BET)","route":"/technologies/epigenetic-drugs/"}],"drug":[{"id":"azacitidine","kind":"drug","name":"Azacitidine","route":"/drugs/azacitidine/"},{"id":"venetoclax","kind":"drug","name":"Venetoclax","route":"/drugs/venetoclax/"}],"roadmap":[{"id":"epigenetics-roadmap","kind":"roadmap","name":"Epigenetic therapy roadmap: loosening silenced genes → mutation-specific enzymes → editing the epigenome","route":"/roadmaps/epigenetics-roadmap/"}]}}