DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for sweat gland disease — screening already-approved drugs against its 14-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleSweat gland disease maps to a 14-gene Open Targets module — the target space DeCure's AI scientist screens approved drugs against.
DeCure.ai methodSignature reversal (LINCS) plus network proximity (STRING) rank already-approved drugs likely to perturb this module — the same engine that produces DeCure.ai's repurposing hypotheses.
Repurposing thesisScreening approved medicines against this disease module, then publishing the evidence for the strongest candidate. Known pharmacology and human exposure data make the first question sharper — they do not establish safety or efficacy in a new indication.
Research record
01
ResearchComing soon
Candidate research + dossier — target rationale, drug-repurposing thesis and evidence pack.proof: Published dossier + on-chain hash
02
ValidationComing soon
In-vitro biological validation at a contract research org (CRO).proof: CRO contract + in-vitro report
03
Peer review & paperComing soon
Peer-reviewed paper published open-access (preprint + journal).proof: DOI + open-access link + on-chain hash
Current lead
No approved-drug candidate for sweat gland disease is corroborated in the literature DeepSearch retrieved. Some conditions are managed with non-pharmacological care — a device, surgery or physical therapy — rather than a medicine; that may be the case here, or the literature we found may simply be too sparse yet to support a drug-repurposing angle.
Molecular view
cordon-bleu WH2 repeat protein (COBL) — COBL is one of the genes genetically linked to this disease in Open Targets — shown as context, not as a drug target we're pursuing: no approved-drug candidate for this disease is yet corroborated in the literature we found.
Loading structure…
helix sheet atpdrag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4PL8 · 2.0 Å · ligand ADENOSINE-5'-TRIPHOSPHATE (ATP). Experimental structure, not a prediction.
What the evidence adds up to
A 1953 review established that all sweat-retention disorders, from miliaria to a wide variety of common dermatological disturbances, result from a simple mechanical obstruction at the sweat duct opening. Sweat is trapped and retained within the skin because its free egress onto the surface is prevented. The same paper noted that for many years these clinical facets of sweat retention went unrecognised or were misdiagnosed.
A 2011 surgical study compared thoracoscopic sympathicotomy at the third rib (R3, 39 cases) versus the fourth rib (R4, 94 cases) for palmar and axillary hyperhidrosis. Early satisfaction was 94.9% in the R3 group and 98.9% in the R4 group, with no significant difference. Late satisfaction was 84.6% for R3 and 89.4% for R4. Recurrence rates were nearly identical: 17.9% for R3 and 17.0% for R4. The only statistically significant difference was in compensatory sweating, which occurred in 71.8% of R3 patients but only 33% of R4 patients (p=0.002). A 2024 review lists the available treatments for hyperhidrosis: topical aluminium salts and formaldehyde, iontophoresis, surgical destruction of sweat glands, transthoracic endoscopic sympathectomy, percutaneous radiofrequency sympathectomy, botulinum toxin injections, and systemic anticholinergic drugs. It mentions the Russian drug Formagel (3.7% formaldehyde) as a non-invasive, effective, safe method.
Two papers address sweat gland regeneration. A 2014 overview describes newly identified reservoirs of stem cells in glandular skin and their activation in response to different types of injuries, but does not report any clinical reconstitution of functional glands. A 2022 Chinese review states that the damage of sweat glands in patients with extensive deep burns results in loss of thermoregulation and that the mechanism of human sweat gland development has not been fully clarified. It notes that cascaded signalling pathways (Wnt/β-catenin, ectodysplasin A/receptor, sonic hedgehog, forkhead box transcription factor) affect sweat gland development and that it has been reported these pathways can be used to achieve reconstruction of sweat adenoid cells in vitro. No in vivo or human reconstitution data are provided.
What is still missing is any controlled trial of a drug specifically repurposed for sweat gland disease, a reliable method to regenerate functional sweat glands in humans, and patient stratification beyond the surgical distinction between R3 and R4 sympathicotomy. The basic obstacle—mechanical duct obstruction—identified in 1953 has not been addressed by any pharmacological intervention tested in a randomised trial.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Cold Spring Harbor Perspectives in Medicine · 2014 · 159 citations · open access
Sweat Gland Progenitors in Development, Homeostasis, and Wound Repair
AbstractThe human body is covered with several million sweat glands. These tiny coiled tubular skin appendages produce the sweat that is our primary source of cooling and hydration of the skin. Numerous studies have been published on their morphology and physiology. Until recently, however, little was known about how glandular skin maintains homeostasis and repairs itself after tissue injury. Here, we provide a brief overview of sweat gland biology, including newly identified reservoirs of stem cells in glandular skin and their activation in response to different types of injuries. Finally, we discuss how the genetics and biology of glandular skin has advanced our knowledge of human disorders associated with altered sweat gland activity.
Clinical and Experimental Dermatology · 2004 · 83 citations
Miliaria crystallina in an intensive care setting
AbstractDrop-like, transient blisters of miliaria crystallina may develop with focal intensity of heat within the skin, such as occurs in tropical climates or during febrile episodes. Miliaria crystallina develops due to a transient poral closure of the sweat duct opening, resulting in obstruction of free flow of eccrine sweat and retention in a vesicle below the skin surface. Dual cholinergic and adrenergic sweat gland innervation is influenced by a variety of medications used in intensive care patients. We present two febrile intensive care patients in whom enhanced alpha-adrenergic stimulation of sweat gland myoepithelia may have led to miliaria crystallina.
The Korean Journal of Thoracic and Cardiovascular Surgery · 2011 · 20 citations · open access
The Effect of Thoracoscopic Sympathicotomy at the Fourth Rib (R4) for the Treatment of Palmar and Axillary Hyperhidrosis
AbstractBACKGROUND: Video-assisted thoracic sympathicotomy plays an important for the treatment of essential hyperhidrosis. Patients are usually satisfied with the surgical outcome at the early post-operative period, but suffer recurrence and compensatory sweating in the late post-operative period. There are many sympathicotomy methods to minimize recurrence and compensatory sweating. We compared the outcome of sympathicotomy methods above the third rib (R3) and the fourth rib (R4) with regards to symptoms, satisfaction, recurrence, and compensatory palmar and axillary hyperhydrosis. MATERIALS AND METHODS: From January 1999 to April 2009, 39 cases of thoracoscopic sympathicotomy at the third rib (R3), and 94 cases of thoracoscopic sympathicotomy at the fourth rib (R4) for palmar and axillary hyperhidrosis were compared for early and late post-operative satisfaction, compensatory sweating and recurrence. RESULTS: There was no sex or age difference between groups. Early satisfaction was 94.9% and 98.9% in the R3 group and R4 group, respectively. There was no difference in early satisfaction (94.9% in R3 and 98.9% in R4), late satisfaction (84.6% in R3 and 89.4% in R4), or recurrence (17.9% in R3 and 17.0% in R4) between groups. There was significant difference in compensatory sweating (71.8% in R3 and 33% in R4, p=0.002). CONCLUSION: R4 sympathicotomy demonstrated superior efficacy in the treatment of compensatory sweating compared to R3 in palmar and/or axillary hyperhidrosis.
AbstractThe physiological significance of the millions of sweat glands spread over the body surface is well known and appreciated, although there has been a general failure to recognize the significance of these tiny glands in the pathogenesis of skin disease. Studies in the last 10 years have indicated clearly that the sweat gland is either primarily or secondarily responsible for a wide variety of common dermatological disturbances. All of the disturbances result from a simple mechanical obstruction at the sweat duct opening; although the formation of sweat proceeds unimpeded, the free egress of this sweat onto the skin surface is prevented. In consequence, sweat is trapped and retained within the skin, leading to a remarkably varied clinical patterning. For many years, these clinical facets of sweat retention went unrecognized or were misdiagnosed. It is now possible to define more precisely and simply the clinical features and the pathogenesis of cutaneous
[Research advances on signaling pathways affecting sweat gland development and their involvement in the reconstitution of sweat adenoid cells in vitro].
AbstractThe damage of sweat glands in patients with extensive deep burns results in the loss of thermoregulation, which seriously affects the quality of life of patients. At present, there are many researches on the repair of sweat gland function, but the mechanism of human sweat gland development has not been fully clarified. More and more studies have shown that the cascaded pathways of Wnt/β-catenin, ecto- dysplasin A/ectodysplasin A receptor/nuclear factor-κB, sonic hedgehog, and forkhead box transcription factor jointly affect the development of sweat glands, and it has been reported that the cascaded signaling pathways can be used to achieve the reconstruction of sweat adenoid cells in vitro. This article reviews the signaling pathways that affect the development of sweat glands and their involvement in the reconstruction of sweat adenoid cells in vitro.
Vestnik dermatologii i venerologii · 2024 · 1 citations · open access
Hyperhidrosis: problems and solutions
AbstractThe functional role of sweating is not limited only to thermoregulation and excretion. There are other functions of it — the ability to enhance and maintain hydration and barrier function of the skin. Excessive sweating can lead to an exacerbation or cause many skin diseases, form psychological discomfort in a person due to wet clothes or an accompanying unpleasant odor. Primary hyperhidrosis may be an autosomal dominant genetic disease. Secondary, usually generalized hyperhidrosis is often associated with drug effects on the body or a systemic disease. The following approaches are used in the treatment of hyperhidrosis: 1) blocking the release of sweat to the skin surface (aluminum salts and formaldehyde); 2) physiotherapy (iontophoresis); 3) destruction of sweat glands and cessation of sweat production (excision of a skin flap with subcutaneous fat, curettage, microwave technology, etc.); 4) termination of the signal from the central nervous system to the sweat glands (transthoracic endoscopic sympathectomy, percutaneous radiofrequency sympathectomy, botulinum toxin injections, systemic anticholinergic drugs). External remedies for excessive sweating include the Russian drug Formagel®, containing 3.7% formaldehyde. This drug is a non-invasive, easily doable, effective, safe method of treating hyperhidrosis.
International Journal of Science and Research (IJSR) · 2024 · 0 citations · open access
A Homoeopathic Approach on Hyperhidrosis of Palm of Hand and Sole of Feet - A Case Report
AbstractHyperhidrosis is a disorder of sweat glands characterized by overproduction of sweat, which is inadequate to the thermoregulatory needs of the body system.Owing to the heavy social and economic burden of the disproportionate perspiration, current treatment methods still do not seem to be sufficient enough to reach patients' expectations.Therefore, the researchers continue a robust pursuit of novel therapy modalities such as topical treatment methods, oral agents, minimally-invasive medical approach and surgical techniques.In this review article authors summarise the disease outline with the emphasis on the new era of hyperhidrosis treatment methods.
Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
DeCure is a research and publication project, not medical advice and not a treatment. "DeCure for X" describes a research goal, not a claim that a cure exists. Backing a cure is a contribution to fund the research — it is not an investment, and confers no yield, royalty, equity or IP ownership. Papers are published open-access by the DeCure.ai DAO.
