DeCure for Isolated growth hormone deficiency type II
DeCure's autonomous Rare AI scientist is researching a drug-repurposing hypothesis for isolated growth hormone deficiency type II — screening already-approved drugs against its 3-gene Open Targets disease module to publish open-access research. Research is fast; the path to publication is funded in milestone stages.
Disease moduleIsolated growth hormone deficiency type II maps to a 3-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
approvedMelatoninMelatonin receptor agonist
Structures already discussed alongside isolated growth hormone deficiency type ii in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
Molecular view
Crystal structure of fad quinone reductase 2 — Melatonin has a real, experimentally solved structure in complex with this target (PDB 4QOG, 1.4 Å). This is the drug's own deposited structure, not a prediction, and confirms it is a structurally characterised molecule rather than an untested guess.
Loading structure…
helix sheet ml1drag to rotate · scroll to zoom
RCSB Protein Data Bank · entry 4QOG · 1.4 Å · ligand Melatonin (ML1). Experimental structure, not a prediction.
What the evidence adds up to
Oral administration of 1 gram of melatonin caused rapid and significant elevations of serum human growth hormone in eight out of nine normal male subjects in a 1974 study. The mean peak growth hormone response was 22.9 ± 4.6 microunits per millilitre. The authors suggested the increased secretion might be due to interaction of melatonin with hypothalamic serotoninergic receptors.
A 1977 study compared intermittent treatment with human growth hormone (one year on, one year off, subsequent years on) to continuous treatment in growth hormone deficient children. The continuous group had a significantly better mean growth response. The reduction in treatment velocity in years after the first was not prevented by the year off treatment; the mean velocity of the intermittent group in their third year was the same as that of the continuous group in their second. The authors concluded intermittent therapy is of less value than continuous treatment and should be avoided.
A 1981 report described a family with isolated growth hormone deficiency in two children, their mother, and presumably two maternal uncles and their maternal grandmother. Autosomal dominant inheritance was the best explanation. The authors noted isolated growth hormone deficiency is a heterogeneous condition including autosomal dominant, autosomal recessive, and non-genetic forms.
A 2016 study measured urinary 6-sulfatoxymelatonin excretion in 12 untreated adults with growth hormone deficiency, 20 treated adults with growth hormone deficiency, and 16 healthy controls. In males, untreated patients had significantly lower total and nocturnal 6-sulfatoxymelatonin than controls, and treated patients showed significantly higher nighttime-daytime delta values than untreated patients. In females, no significant differences were found among the three groups. Significant correlations were found between 6-sulfatoxymelatonin measures and serum IGF-1 levels in both sexes. A 2024 review summarised that inadequate diagnosis and treatment of transition growth hormone deficiency remains a major clinical concern, and that international guidelines have been developed to address it. What is still missing is prospective trial data that stratifies patients by genetic subtype, particularly for the autosomal dominant form, and funding for studies that test whether melatonin or other chronobiological interventions alter growth hormone secretion in a clinically meaningful way.
Evidence
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
Science · 1974 · 77 citations
Growth Hormone Responses to Melatonin in Man
AbstractOral administration of 1 gram of melatonin caused rapid and significant elevations of serum human growth hormone in eight out of nine normal male subjects. The mean (+/- standard error of the mean) of the peak response by growth hormone was 22.9 +/- 4.6 microunits per milliliter. The increased secretion of growth hormone may be due to interaction of melatonin with hypothalamic serotoninergic receptors.
The Journal of Clinical Endocrinology & Metabolism · 1977 · 12 citations
Results of Intermittent Treatment of Growth Hormone Deficiency with Human Growth Hormone
AbstractThe growth in stature of two groups of growth hormone deficient children has been compared. The frist group received intermittent treatment with human Growth Hormone (hGH), 1 year on, 1 year off, subsequent years on; the second group received continous treatment. This latter group had a significantly better mean growth response. The reduction in treatment velocity in years subsequent to the first was not prevented by the year off treatment, the mean velocity of the intermittent group in their 3rd year being the same as that of the continous group in their second. We conclude that intermittent hGH therapy is of less values than continous treatment and should be avoided, at least pending further evidence.
AbstractA family is reported with isolated growth hormone deficiency in two children, their mother and, presumably, also in two maternal uncles and their maternal grandmother. Autosomal dominant inheritance is the best explanation. Isolated growth hormone deficiency is apparently a heterogeneous condition, including autosomal dominant, autosomal recessive as well as non-genetic diseases.
Greater South Information System · 2016 · 0 citations · open access
Male-female differences in 6-sulfatoxymelatonin excretion in hypopituitary patients
AbstractTo evaluate melatonin secretion in adult hypopituitary patients with Growth Hormone deficiency (AGHD) on and off replacement therapy.We studied 48 subjects: 12 (6 males) untreated AGHD (AGHDnt), 20 (10 males) treated AGHD (AGHDt) and 16 healthy subjects (8 males) as control group (CG). We measured urinary 6-sulfatoxymelatonin (6-SM) in total (24 h samples), nocturnal (6-SMn): 1800-0800 and diurnal samples (6-SMd): 0800-1800.Significant differences were observed among the 3 groups of male subjects, in total 6-SM (p < 0.05), nocturnal 6-SM (p < 0.02) and nighttime-daytime delta values (p < 0.003). CG had significantly higher values than the AGHDnt in total 6-SM (p < 0.01), nocturnal 6-SM (p < 0.05) and nighttime-daytime delta values (p < 0.01). AGHDt patients showed significantly higher levels in nighttime-daytime delta values than AGHDnt patients (p < 0.05). In females, no significant differences were found among the 3 groups studied in total, nocturnal, diurnal or nighttime-daytime delta values. In males, significant correlations were found among total 6-SM (r = 0.58; p = 0.029), nocturnal 6-SM (r = 0.70; p = 0.006) and nighttime-daytime delta values (r = 0.71; p = 0.004) vs. serum IGF-1 levels in subjects evaluated. In females, significant correlations were found among total 6-SM (r = 0.57; p = 0.02) vs. serum IGF-1 levels in subjects evaluated. A tendency towards a significant correlation was found in diurnal 6-SM (r = 0.48; p = 0.07).Our findings show a sexual dimorphism in 6-SM excretion in AGHD patients and provide an interesting approach to a further understanding of some chronobiological disorders involved in GH deficiency.
[Management of transition growth hormone deficiency].
AbstractWith an increasing understanding of growth hormone deficiency, there has been a growing emphasis on the management of transition growth hormone deficiency (TGHD) in clinical practice. The inadequate diagnosis and treatment of TGHD have been a major clinical concern, leading to the development of relevant guidelines and consensus internationally. This article summarizes the evaluation, diagnosis, treatment, and clinical challenges of TGHD based on these guidelines, consensus, and existing clinical studies, aiming to optimize and further improve the clinical diagnosis, treatment, and management of TGHD.
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.
