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melatonin

✓ Approved

Clinigen Group · MTNR1A · 小分子

什么是 melatonin？

melatonin 是一种小分子，由Clinigen Group研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

公司Clinigen Group
药物类别小分子
分子靶点MTNR1A, MTNR1B
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Clinigen Group

作用机制

分子靶点

melatonin 作用于 2 个分子靶点：

MTNR1Amelatonin receptor 1A (MEL-1A-R, MT1)
MTNR1Bmelatonin receptor 1B (FGQTL2, MT2)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

melatonin 针对 2 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Psychiatric disordersInsomnia✓ Approved
Psychiatric disordersSleep disorder✓ Approved

相关研究文献

PubMedScience progress2026-10-26

Melatonin attenuates diquat-induced acute liver injury by modulating Nrf2-Associated antioxidant signaling and ferroptosis-related processes.

Xia Lei L, Liu Guanghe G, Duan Yunpeng Y, Dong Yuxin Y et al.

ObjectiveDiquat (DQ) poisoning can cause severe acute liver injury associated with oxidative stress. This experimental animal study investigated the involvement of ferroptosis-related processes and Nrf2-associated antioxidant signaling in the protective effects of melatonin against DQ-induced liver injury.MethodsMale C57BL/6J mice were used in an experimental DQ-induced acute liver injury model. DQ was administered intraperitoneally, with an LD50 of 42.70 mg/kg and 24 h selected as the peak-injury time point. Liver injury, inflammation, oxidative stress, iron homeostasis, mitochondrial damage, ferroptosis-related markers, and Nrf2 signaling were assessed. RSL3 and ML385 were used to challenge ferroptosis-related protection and inhibit Nrf2 signaling, respectively. Nrf2 nuclear accumulation, HO-1, NQO1, SLC7A11, and FSP1 were additionally evaluated. A post-exposure experiment tested melatonin administered 2 h after DQ.ResultsDQ increased serum ALT and AST, inflammatory cytokines, ROS, lipid peroxidation, and hepatic Fe2+ accumulation, while decreasing GSH and impairing mitochondrial function and morphology (all P < 0.05). DQ also reduced GPX4, FTH1, SLC7A11, and FSP1 and increased ACSL4 and TFR1. Melatonin significantly attenuated these changes, enhanced Nrf2 nuclear accumulation, and increased HO-1 and NQO1 expression. RSL3 weakened melatonin-associated protection and partially reversed improvements in liver injury, inflammation, Fe2+ accumulation, MDA, GSH, and GPX4. ML385 similarly attenuated Nrf2 nuclear accumulation, HO-1/NQO1 expression, restoration of SLC7A11 and FSP1, and protection against liver injury and ferroptosis-related alterations (P < 0.05 vs. FMDQ). Post-exposure melatonin also reduced ALT, AST, and histological liver injury.ConclusionsMelatonin attenuates DQ-induced acute liver injury. Pharmacological findings support contributions of Nrf2-associated antioxidant signaling and suppression of oxidative stress and ferroptosis-related processes, although they do not establish an exclusive causal pathway. Post-exposure efficacy further supports the potential translational relevance of melatonin.

PMID 42929063
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PubMedAnnals of the New York Academy of Sciences2026-10-26

Bidirectional Interaction Between Clock Genes and Reactive Oxygen Species Production in Carp and Zebrafish Macrophages.

Mazur Mikolaj M, Baran Zaneta Z, Klak Katarzyna K, Maciuszek Magdalena M et al.

Our study investigated the bidirectional interaction between circadian clock genes and reactive oxygen species (ROS) production in fish monocytes/macrophages (Mo/Mf). Macrophages are key leukocytes whose antimicrobial activity relies on ROS generation. As ROS levels fluctuate across the day and clock genes regulate numerous cellular processes, we examined whether macrophage clock gene activity and ROS production are functionally interconnected. We found that carp Mo/Mf displayed constitutive expression of core clock genes and genes involved in melatonin synthesis and redox balance: Clock genes (per2, clock, cry2, and bmal2) showed rhythmic expression under both light:dark and constant dark conditions and ROS production varied across the day. Ex vivo cell stimulation revealed that immune signals, cortisol, and ROS‑modulating agents altered clock gene expression. Direct ROS donors upregulated multiple clock genes, while inhibition of NADPH oxidase reduced ROS production and changed expression of clock genes. Finally, zebrafish mutants lacking cry1 exhibited changes in ROS production, demonstrating that disruption of the circadian clock affects redox activity. Together, these findings show that carp and zebrafish Mo/Mf possess a functional circadian system and that the ROS and clock pathways influence each other. This interplay may shape daily patterns of immune responsiveness and contribute to time‑dependent variation in host defense.

PMID 42929052
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PubMedMuscles (Basel, Switzerland)2026-10-25

Melatonin and Cisplatin-Associated Skeletal Muscle Wasting and Atrophy: Mechanistic Rationale, Current Evidence, and Research Gaps.

Hassan Mohamed A A MAA, Abd-Elnaeim Mahmoud M, Abd-Elhafez Enas A EA, Sayed Ramy K A RKA

Cisplatin causes skeletal muscle wasting in tumor-free rodents, reducing muscle mass, myofiber size and, where measured, strength. This critical narrative review appraises that phenotype and its mechanistic basis. Tumor-bearing models show that the loss also occurs under tumor burden, but most cannot separate drug from tumor effects. Melatonin influences mitochondrial, redox, regenerative, and structural outcomes in skeletal muscle under non-cisplatin conditions. Direct melatonin-cisplatin evidence is limited to pretreatment studies in C2C12 cells from one research group. No in vivo melatonin-plus-cisplatin skeletal-muscle study and no clinical study of melatonin against cisplatin-associated muscle loss were identified in searches through 22 September 2026. Biological plausibility is supported, but protection has not been demonstrated. A controlled tumor-free study would provide a more interpretable test of whether melatonin protects skeletal muscle during cisplatin exposure. Translational validation would then require a separate tumor-bearing study testing whether protection persists under tumor burden and whether cisplatin's antitumor activity is preserved.

PMID 42924648
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PubMedFrontiers in bioengineering and biotechnology2026-10-25

A melatonin textile transdermal patch based on physicochemical synergistic permeation-enhancement strategy for circadian rhythm regulation.

Zhao Juyang J, Liu Jinzhi J, Lin Jiahan J, Liu Mingtao M et al.

Melatonin, an endogenous circadian rhythm-regulating hormone, has faced challenges in achieving prolonged exogenous regulation due to its low oral bioavailability and short half-life. Existing transdermal strategies are difficult to balance efficacy, safety, and accessibility. To address this, we propose a physicochemical synergistic permeation-enhancement strategy and have developed a melatonin textile transdermal patch based on the synergistic action of electret and permeation enhancer. The patch is designed with a three-layer composite structure, composed of a textile-based electret backing layer, a drug-loading pressure sensitive adhesive layer containing melatonin and permeation enhancer, and a protective layer to prevent drug leakage. Electret and permeation enhancer enhance transdermal efficiency through a physicochemical synergistic permeation-enhancement strategy without disrupting the skin barrier. In vitro studies revealed that among various permeation enhancers (menthol, azone, oleic acid) and electret parameters, the combination of a -1500 V electret with 10% oleic acid exhibited the optimal synergistic effect. In vivo pharmacokinetic studies demonstrated that the patch reached a peak plasma concentration (>30 ng/mL) within 1 h and maintained effective therapeutic levels (>5 ng/mL) for up to 8 h. The patch significantly improved the sleep quality in insomniac rats, with no observed skin irritation or cytotoxicity. This study not only accomplishes an efficient, non-invasive, and parametrically tunable transdermal delivery of melatonin but also validates the feasibility of synergistic enhancement through physical field regulation and chemical permeation, thereby providing a viable strategy for developing safe and long-acting textile-based transdermal drug delivery systems aimed at neuroendocrine small-molecule hormones similar to melatonin.

PMID 42922935
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PubMedJournal of pineal research2026-10-25

Persistent Endothelial Glycocalyx Disruption in Sepsis: Translational Evidence for Melatonin-Mediated Vascular Protection.

Martín-Estebané María M, Acuña-Fernández Carlos C, López-Soto Pablo J PJ, Hernández-Belsmeisl Jessica J et al.

Sepsis is a life-threatening syndrome driven by a dysregulated host response to infection, with endothelial dysfunction and glycocalyx disruption playing central roles in vascular failure. Despite growing recognition of the glycocalyx as a therapeutic target, its temporal dynamics and potential pharmacological modulation remain poorly understood. We performed a translational study combining longitudinal clinical observations in septic patients with mechanistic investigations in a murine cecal ligation and puncture (CLP) model. Plasma from patients was collected at intensive care unit admission and after clinical recovery to assess inflammatory mediators, coagulation parameters, and glycocalyx-related biomarkers. In parallel, the CLP model evaluated systemic and tissue-specific glycocalyx alterations and the effects of injectable melatonin. Acute sepsis induced marked alterations in multiple glycocalyx-related biomarkers in patients, with several changes persisting despite normalization of organ dysfunction and standard inflammatory indices, indicating ongoing endothelial injury and repair. In the CLP model, sepsis reproduced these alterations, while melatonin treatment significantly attenuated systemic cytokine responses and partially restored circulating and tissue glycocalyx components in an organ- and gene-specific manner. These results highlight persistent, dynamic glycocalyx disruption as a key driver of sepsis pathology and support pharmacological stabilization of the glycocalyx as a promising therapeutic strategy. Melatonin emerges as a potential endothelial-protective agent capable of promoting vascular recovery and homeostasis, providing translational insight for interventions targeting microvascular integrity in sepsis.

PMID 42927469
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PubMedACS omega2026-10-25

Establishing an in Vitro Model of Astrocyte Activation in Ischemic Traumatic Brain Injury: Therapeutic Synergy of Melatonin and Oxygen Nanobubbles.

Igbalaye Jimoh Olamilekan JO, Jain Shreyaan S, Wenning Elizabeth E, Bushra Anika A et al.

Secondary injury following ischemic traumatic brain injury (TBI) is heavily driven by neurovascular dysfunction involving endothelial damage, astrocyte reactivity, inflammation, and hypoxic stress, among other contributing pathophysiological processes. Here, we establish a mechanistically informative in vitro ischemic TBI model that isolates endothelial-astrocyte crosstalk using human brain microvascular endothelial cells (HBMECs) and astrocytes. Using this platform, we evaluated melatonin and oxygen nanobubbles (ONBs) as a combinatorial therapeutic strategy. Fabricated ONBs exhibited a mean hydrodynamic diameter of 78.35 ± 0.42 nm, a negative surface charge of -37.86 ± 1.32 mV, and sustained oxygen retention (56.38 ± 0.86 mg/L initially). Mechanical needle-scratch injury combined with hypoxia induced primary endothelial injury characterized by reduced viability and increased expression of inflammatory and hypoxia-associated markers, quantified by quantitative real-time PCR (qRT-PCR). Injured HBMECs subsequently triggered astrocyte reactivity marked by elevated GFAP (1.93-fold; p < 0.0001), NLRP3 (3.21-fold; p < 0.0001), NF-κβ signaling (1.62-fold; p < 0.0001), and HIF-1α (2.28-fold; p < 0.0001), while reactive astrocytes propagated a secondary wave of endothelial degeneration, establishing a bidirectional injury loop. Melatonin alone only partially mitigated injury-associated signaling, whereas the melatonin-ONBs combination restored astrocytic and endothelial gene expression to near-baseline levels. These findings highlight a multimodal therapeutic approach that effectively suppresses inflammatory, apoptotic, and hypoxic signaling in ischemic TBI.

PMID 42923425
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