<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>26(18)</volume><submitter>Tan IJ</submitter><pubmed_abstract>Chronic inflammatory disorders of the apocrine gland (CIDAP), such as hidradenitis suppurativa (HS), are characterized by painful, recurrent lesions in apocrine gland-rich areas. First-line treatments-including retinoids and antibiotics-often fail to prevent recurrence and biofilm formation, necessitating the use of targeted biologic therapies. This review evaluated U.S.-based randomized controlled trials and cohort studies published between 2014 and 2024 on the efficacy of such therapies in adult HS patients. A total of 13 studies met inclusion criteria. Agents targeting interleukins (IL-17A, IL-17F, IL-23, IL-1α, IL-36) and TNF-α were assessed, with outcomes including HiSCR, Sartorius scores, DLQI, and patient-reported measures. IL-17 inhibitors (secukinumab, bimekizumab) and IL-1 inhibitors (bermekimab, anakinra) demonstrated promising reductions in inflammatory burden and improved quality of life. TNF-α inhibitors, particularly adalimumab and infliximab, consistently achieved HiSCR and HSS improvements. Guselkumab (IL-23) showed limited efficacy in HiSCR but modest pain relief. Safety profiles were generally acceptable across agents, with few serious adverse events. Limitations across studies included small sample sizes, lack of control arms, and short follow-up durations. These findings underscore the therapeutic potential of biologic agents in managing HS. A greater emphasis on biomarker-guided treatment selection and interdisciplinary collaboration is warranted to optimize long-term outcomes for patients.</pubmed_abstract><journal>International journal of molecular sciences</journal><pagination>8887</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12469770</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Targeted Biologic Therapies for Hidradenitis Suppurativa.</pubmed_title><pmcid>PMC12469770</pmcid><pubmed_authors>Tan IJ</pubmed_authors><pubmed_authors>Agarwal P</pubmed_authors><pubmed_authors>Wolfe SM</pubmed_authors><pubmed_authors>Cohen BA</pubmed_authors><pubmed_authors>Nguyen HN</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeted Biologic Therapies for Hidradenitis Suppurativa.</name><description>Chronic inflammatory disorders of the apocrine gland (CIDAP), such as hidradenitis suppurativa (HS), are characterized by painful, recurrent lesions in apocrine gland-rich areas. First-line treatments-including retinoids and antibiotics-often fail to prevent recurrence and biofilm formation, necessitating the use of targeted biologic therapies. This review evaluated U.S.-based randomized controlled trials and cohort studies published between 2014 and 2024 on the efficacy of such therapies in adult HS patients. A total of 13 studies met inclusion criteria. Agents targeting interleukins (IL-17A, IL-17F, IL-23, IL-1α, IL-36) and TNF-α were assessed, with outcomes including HiSCR, Sartorius scores, DLQI, and patient-reported measures. IL-17 inhibitors (secukinumab, bimekizumab) and IL-1 inhibitors (bermekimab, anakinra) demonstrated promising reductions in inflammatory burden and improved quality of life. TNF-α inhibitors, particularly adalimumab and infliximab, consistently achieved HiSCR and HSS improvements. Guselkumab (IL-23) showed limited efficacy in HiSCR but modest pain relief. Safety profiles were generally acceptable across agents, with few serious adverse events. Limitations across studies included small sample sizes, lack of control arms, and short follow-up durations. These findings underscore the therapeutic potential of biologic agents in managing HS. A greater emphasis on biomarker-guided treatment selection and interdisciplinary collaboration is warranted to optimize long-term outcomes for patients.</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Sep</publication><modification>2026-05-02T03:19:24.641Z</modification><creation>2026-05-02T03:11:45.141Z</creation></dates><accession>S-EPMC12469770</accession><cross_references><pubmed>41009454</pubmed><doi>10.3390/ijms26188887</doi></cross_references></HashMap>