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melatonin

✓ Approved

Clinigen Group · MTNR1A · Small Molecule

What is melatonin?

melatonin is a small molecule developed by Clinigen Group. It is approved for therapeutic indications via oral (po).

Drug Profile

CompanyClinigen Group
Drug ClassSmall Molecule
Molecular TargetMTNR1A, MTNR1B
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Clinigen Group

Mechanism of Action

Molecular Targets

melatonin acts on 2 molecular targets:

MTNR1Amelatonin receptor 1A (MEL-1A-R, MT1)
MTNR1Bmelatonin receptor 1B (FGQTL2, MT2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

melatonin is developed for 2 unique indications across 1 therapeutic area.

Therapeutic AreaConditionPhase
Psychiatric disordersInsomnia✓ Approved
Psychiatric disordersSleep disorder✓ Approved

Related Research Articles

PubMedBrazilian journal of otorhinolaryngology2026-10-14

Cochlear histological changes after noise exposure: effects of melatonin and resveratrol in an experimental model.

Novanta Gabriela Guenther Ribeiro GGR, Zica Ana Carolina Odorizzi ACO, Sampaio Maria Luiza Queiroz MLQ, Caram Andressa Alves AA et al.

To assess cochlear histological changes and the otoprotective effects of melatonin and resveratrol in Wistar rats exposed to high sound pressure levels. This was a prospective, longitudinal, in vivo experimental study with heterogeneous male Wistar rats. The animals were divided into groups and treated with or without 10 mg/day of melatonin or resveratrol administered intraperitoneally for 14 days. They were then exposed to or not exposed to white noise (4 kHz; 100 ± 3 dB) for 8 h daily for 10-days. Histological analyses were performed on the spiral ganglion, spiral limbus, spiral ligament, and stria vascularis on days 15 (D15) and 30 (D30), after euthanasia. The data were analyzed by ANOVA. The animals in the control group had a higher number of cells in the analyzed cochlear structures than the noise-exposed group. Treatment with melatonin or resveratrol prevented the noise-induced reduction in the number of neurons in the spiral ganglion, maintaining cell counts similar to those in the control group. Resveratrol was also effective in preserving the spiral ligament. The findings suggest that the preventive administration of antioxidants may be an effective strategy in mitigating noise-induced hearing loss, reinforcing the therapeutic potential of these compounds in preventing hearing impairment. V.

PMID 42874301
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PubMedFrontiers in neurology2026-10-14

Correlation of peripheral blood BMAL1 level with non-motor symptoms in Parkinson's disease patients.

Jiang Yanyan Y, Zhang Yufei Y, Dong Luoqing L, Zhu Hongcan H

This study aimed to quantify BMAL1 expression in the peripheral blood of patients with Parkinson's disease (PD) and to evaluate its correlation with non-motor symptoms (NMS). We further assessed whether serum interleukin-6 and melatonin levels were associated with BMAL1 expression. This study included 80 patients with PD and 80 age-and sex-matched healthy controls. General clinical information and scores on multiple NMS scales were collected. Peripheral blood BMAL1 expression was quantified using real-time quantitative polymerase chain reaction. Serum levels of melatonin and interleukin-6 were measured using enzyme-linked immunosorbent assay. Spearman's correlation analysis was used to evaluate the associations between BMAL1 expression and the NMS scores. Compared to healthy controls, patients with PD exhibited significantly lower peripheral blood BMAL1 expression levels in the morning (p = 0.005). BMAL1 levels were negatively correlated with the NMS Scale score (r = -0.407, p < 0.001). Furthermore, higher BMAL1 levels were associated with better night-time sleep quality and cognitive function, whereas lower BMAL1 levels correlated with more severe anxiety and depression. A weak positive correlation was observed between BMAL1 expression and melatonin levels (r = 0.267, p = 0.017). A significant negative correlation was found between BMAL1 expression and interleukin-6 level (r = -0.603, p < 0.001). In this cross-sectional study, peripheral blood BMAL1 expression at a single morning time point was lower in patients with PD and correlated with NMS severity, suggesting a potential pathway involving BMAL1, melatonin, and inflammatory cytokines in NMS pathogenesis. Future studies with multiple time-point measurements are required to validate these findings.

PMID 42871215
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PubMedFunctional plant biology : FPB2026-10-14

Combined application of melatonin and salicylic acid improves drought tolerance in pepper (Capsicum annuum) through coordinated physiological and biochemical responses.

Köklü Ardıç Şebnem Ş

Drought stress is a major environmental constraint limiting growth, water relations, and metabolic stability in pepper (Capsicum annuum). This study evaluated the individual and combined effects of melatonin (MEL) and salicylic acid (SA) on drought tolerance by assessing growth, water status, photosynthetic pigments, oxidative stress markers, osmotic adjustment, and antioxidant defence systems. Plants were grown under non-stressed and drought-stressed conditions and treated with MEL, SA, or their combination. Drought stress significantly reduced fresh weight, relative water content, and photosynthetic pigments, while increasing accumulation of hydrogen peroxide and malondialdehyde, indicating severe oxidative damage. Exogenous application of MEL and SA alleviated these effects, with the combined treatment providing the greatest protection. Under drought, the combined application improved biomass accumulation and tissue hydration, preserved chlorophyll and carotenoid contents, reduced oxidative damage, and increased proline accumulation. It also markedly increased superoxide dismutase, catalase, and peroxidase activities, showing enhanced detoxification of reactive oxygen species. These findings demonstrate that the greater drought tolerance conferred by the combined treatment is associated with coordinated regulation of water balance, redox homeostasis, osmotic adjustment, and photosynthetic stability. The combined application of MEL and SA is a promising strategy for improving drought tolerance in pepper cultivation.

PMID 42875011
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PubMedNeurochemical research2026-10-14

Melatonin Exerts Neuroprotective Effects in Escherichia coli/Lipopolysaccharide Induced Neuronal Injury via Regulating TFRC-Related Ferroptosis.

Zheng Yihui Y, Zhu Tingyu T, Mao Niping N, Wang Xun X et al.

Neonatal bacterial meningitis (NBM) is a severe neonatal infectious disease associated with a high incidence of neurological sequelae. Lipopolysaccharide (LPS) and inflammatory cytokines aggravate cerebral injury, whereas the mechanism of ferroptosis in the pathogenesis of NBM remains unclear. Melatonin (MT), an endogenous neurohormone, provides anti-ferroptotic neuroprotection in models of cerebral injury; however, its mechanism of action against NBM-related injury through ferroptosis has not been clarified. This study investigated the protective effects mediated by MT in vivo and in vitro. Rat models of LPS-induced inflammatory brain injury were established through intracerebroventricular (i.c.v.) injection, and Escherichia coli (E. coli)-infected cell models were developed to investigate the neuroprotective effects of MT against TFRC-related ferroptosis. CCK-8 assays, Western blotting, transmission electron microscopy (TEM), iron detection, and immunofluorescence, BODIPY staining were used to assess cell viability, inflammatory factors, mitochondrial ultrastructure, iron accumulation, and GPX4 expression. E. coli infection induced typical ferroptotic mitochondrial damage. MT alleviated neuroinflammation and reduced the expression of ferroptosis-related proteins both in vitro and in vivo. MT treatment increased mitochondrial GPX4 expression. The ferroptosis agonist RSL3 reversed the neuroprotective effects of MT. MT inhibited TFRC-related ferroptosis and alleviated neuronal damage. MT protects against E. coli/Lipopolysaccharide induced neuronal injury by regulating TFRC-related ferroptosis, indicating that MT may be a promising therapeutic agent for NBM.

PMID 42873388
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PubMedJournal of vision2026-10-14

Circadian timing does not modulate human temporal contrast sensitivity.

Heinrichs Hannah Sophie HS, Spitschan Manuel M

Previous studies have reported diurnal variations in color perception and luminance contrast sensitivity, suggesting modulation of visual processing by the circadian pacemaker. To clarify potential time-of-day effects, we examined whether cone-mediated temporal contrast sensitivity is modulated by circadian timing. We disentangled circadian and homeostatic influences on human visual performance using a 40-hour forced desynchrony protocol. Twelve participants (five female participants, 24.4 ± 2.9 years, range 19-30) followed a repeating 3.75-hour cycle comprising 2 hours 30 minutes of wakefulness and 1 hour 15 minutes of sleep under constant environmental conditions. Circadian period was estimated from up to 46 salivary melatonin samples per participant. During wake periods, participants repeatedly completed temporal contrast sensitivity tasks at 2 Hz and 8 Hz, using tasks that probed both luminance (L+M+S) and chromatic (L-M, S-cone-directed) modulations. We tested for circadian modulation of visual performance by comparing hierarchical cosinor models with intercept-only null models using Bayes factors. All participants showed robust melatonin rhythms (mean τ = 24.18 ± 0.39 hours). Bayesian inference provided decisive evidence against circadian variation in luminance or chromatic contrast sensitivity. Within this controlled protocol, we found no detectable near-24-hour modulation of cone-mediated temporal contrast sensitivity. Previously reported time-of-day effects may instead reflect homeostatic influences, pupil-linked changes in retinal illuminance, or mechanisms outside the cone-mediated pathways probed here. By separating circadian phase from sleep-wake-related influences, this study clarifies when circadian modulation of visual performance can and cannot be inferred.

PMID 42872932
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PubMedPflugers Archiv : European journal of physiology2026-10-14

Circadian melatonin suppression and vitamin D deficiency disrupt aortic reactivity via MT1/MT2 and VDR-dependent mechanisms in rats.

Shekh Rebaz S RS, Maulood Ismail M IM

Circadian disruption and vitamin D deficiency (VDD) are increasingly prevalent and independently associated with cardiovascular dysfunction. However, their combined impact on vascular reactivity and receptor signaling remains insufficiently defined. This study investigated the independent and interactive effects of melatonin (MEL) suppression induced by continuous light (CL) or pinealectomy (Px) and VDD on vascular contractility, endothelial function, and MT1/vitamin D receptor (VDR) gene expression in rat thoracic aorta. Isolated aortic rings were subjected to cumulative concentration response curves for phenylephrine (PE) and acetylcholine (ACh). Pharmacodynamic parameters, potency (pD₂), maximal efficacy (Emax), and area under the curve (AUC) were calculated. MEL and calcitriol modulation with receptor antagonism was performed to determine receptor dependence. Relative MT1 and VDR mRNA expression was quantified using quantitative reverse transcription polymerase chain reaction (qRT-PCR). CL, Px, and VDD significantly enhanced PE-induced maximal contraction, with the combined deficiency groups exhibiting the greatest augmentation of α₁-adrenergic responsiveness. In contrast, ACh-induced relaxation was selectively impaired under dual-deficiency conditions, characterized by reduced Emax without major changes in pD2, indicating compromised endothelial efficacy rather than altered receptor sensitivity. MEL attenuated vasoconstriction and enhanced relaxation in a receptor-dependent manner, whereas calcitriol potentiated contractility through VDR signaling. Notably, combined CL + VDD produced marked upregulation of MT1 (~ 10-fold) and VDR (~ 108-fold), suggesting compensatory transcriptional remodeling. Circadian disruption and VDD synergistically promote vascular hyperreactivity and endothelial dysfunction. Their convergence amplifies α₁-adrenergic signaling while impairing nitric oxide (NO) mediated relaxation, identifying a mechanistic axis linking modern light exposure and hypovitaminosis D to heightened cardiovascular risk.

PMID 42870116
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