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Depending on the cellular context, p75\n NTR<\/jats:sup>\n can promote trophic or degenerative signaling, which can influence a broad spectrum of pathological conditions, including neurodegenerative diseases, inflammatory\/infectious conditions, and various central and peripheral nervous system injuries. These attributes of p75\n NTR<\/jats:sup>\n and its widespread, frequently upregulated expression on affected cells and tissues, make it a compelling therapeutic target. Among various therapeutic targeting strategies, the first-in-class small molecule p75\n NTR<\/jats:sup>\n modulator, LM11A-31, has emerged as a leading candidate and has been evaluated in 62 published preclinical studies spanning 26 distinct disease and injury models.\n <\/jats:p>\n <\/jats:sec>\n \n Main body<\/jats:title>\n \n This review covers the foundational biology of p75\n NTR<\/jats:sup>\n signaling and expression and all published mechanistic and preclinical studies evaluating LM11A-31, focusing on outcomes that have been reproduced across multiple studies and independent labs. Beyond its therapeutic potential, we also explore how LM11A-31 has served as a powerful pharmacological probe, significantly advancing our knowledge of p75\n NTR<\/jats:sup>\n biology. LM11A-31 consistently reduced elevated JNK\/c-Jun, NF\u03baB, and RhoA signaling, and normalized reduced PI3K\/AKT signaling in a variety of pathological conditions. It also mitigated associated disease processes, including inflammation, degeneration of neurites, synapses, and dendritic spines, and cell death. These protective effects against pathologies often improved functional outcomes, including cognitive and motor measures. Studies using LM11A-31 also uncovered emerging molecular and cellular functions of p75\n NTR<\/jats:sup>\n by demonstrating its ability to improve autophagy, calcium and redox homeostasis, and blood-brain barrier function. Finally, a Phase 2a clinical trial applying LM11A-31 for Alzheimer\u2019s disease demonstrated a favorable safety profile and significantly slowed the progression of biomarkers related to neurodegenerative mechanisms.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Together, these studies expand our understanding of p75\n NTR<\/jats:sup>\n function and support p75\n NTR<\/jats:sup>\n modulation as a promising therapeutic strategy across diverse pathological conditions.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1186\/s12967-026-08276-x","type":"journal-article","created":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T05:31:24Z","timestamp":1779946284000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Taming the \u201cdeath receptor\u201d: translating the first-in-class p75NTR modulator LM11A-31 from basic biology, across broad preclinical models, to clinical proof-of-concept"],"prefix":"10.1186","volume":"24","author":[{"given":"Vanessa F.","family":"Langness","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6122-840X","authenticated-orcid":false,"given":"Danielle A.","family":"Simmons","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sukhneet","family":"Kaur","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen M.","family":"Massa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9514-7325","authenticated-orcid":false,"given":"Frank M.","family":"Longo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,5,28]]},"reference":[{"issue":"4749","key":"8276_CR1","doi-asserted-by":"publisher","first-page":"518","DOI":"10.1126\/science.3008331","volume":"232","author":"MV Chao","year":"1986","unstructured":"Chao MV, Bothwell MA, Ross AH, Koprowski H, Lanahan AA, Buck CR, et al. 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