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Hexarelin Tablets
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Hexarelin Tablets

Hexarelin Tablets

1.General Specification(in stock)
(1)API(Pure powder)
(2)Tablets
(3)Injection
(4)Capsule
2.Customization:
We will negotiate individually, OEM/ODM, No brand, for secience researching only.
Internal Code: BM-2-132
Hexarelin CAS 140703-51-1
Molecular weight: 887.04
EINECS number: 1312995-182-4
Main market: USA, Australia, Brazil, Japan, Germany, Indonesia, UK, New Zealand , Canada etc.
Analysis: HPLC, LC-MS, HNMR
Technology support: R&D Dept.-4

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Hexarelin tablets, as a synthetic growth hormone releasing peptide (GHRP), is the core logic of its auxiliary intervention research for sarcopenia and osteoporosis. It improves muscle mass, muscle strength, and bone tissue homeostasis by specifically regulating growth hormone secretion and bone and muscle metabolism related pathways. Currently, related research mainly focuses on preclinical animal experiments and early exploration. The following two directions are divided into sarcopenia and osteoporosis, and their auxiliary intervention effects and related research basis are explained in detail.

Our Products Description

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Method of Analysis

Hexarelin COA

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Research on Hexarelin as an Adjuvant Intervention for Sarcopenia

Delays Sarcopenia Progression:For age-related sarcopenia and disease-related sarcopenia (such as muscle wasting caused by chronic consumptive diseases), it can inhibit muscle cell apoptosis pathways and increase the rate of muscle protein synthesis. This delays the progressive loss of skeletal muscle and prevents sarcopenia from advancing to severe functional impairment, offering a new direction for intervention research in these refractory types of sarcopenia. 

Core Regulatory Mechanisms like activates the growth hormone secretagogue receptor (GHSR-1a), specifically stimulating the pituitary gland to release growth hormone (GH), which in turn induces the liver to synthesize and secrete insulin-like growth factor-1 (IGF-1). This creates a synergistic regulation via the GH-IGF-1 axis, which is the core pathway for its adjuvant intervention in sarcopenia. It directly mediates positive regulation of muscle metabolism, distinguishing it from other non-GH-dependent regulatory effects.

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It acts directly on GHSR-1a receptors on the surface of skeletal muscle cells, initiating anabolic signaling pathways within myocytes without relying on GH mediation. This promotes muscle cell proliferation and differentiation while inhibiting muscle cell apoptosis and reducing pathological loss of skeletal muscle, providing a dual regulatory pathway for sarcopenia intervention.

Specific Adjuvant Intervention Effects

Increases Muscle Mass and Strength:Promotes protein synthesis in skeletal muscle cells, increases the cross-sectional area of muscle fibers (particularly fast-twitch fiber content), and enhances collagen synthesis and skeletal muscle matrix strength. This addresses the issues of reduced muscle volume and decreased muscle strength in sarcopenia patients or animal models. In a 16-week administration experiment on elderly dogs, Hexarelin tablets improved muscle morphology and biochemical indicators in some test animals, supporting its positive regulatory effect on muscle.

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Improves Muscle Function and Exercise Capacity:Alleviates sarcopenia-related muscle fatigue and decreased exercise endurance. By regulating muscle energy metabolism, it enhances the aerobic metabolic efficiency of skeletal muscle and reduces the recovery period for exercise-induced muscle damage, providing auxiliary support for functional recovery in sarcopenia patients. This aligns with the core goal of "increasing muscle mass + preserving function" in sarcopenia intervention.

 

Current Research Status

Current studies are mainly focused on animal experiments (e.g., elderly rodent and elderly dog models), confirming that Hexarelin can significantly increase muscle mass and strength, and improve muscle morphological indicators in model animals. Large-scale human clinical trials have not yet been conducted. Existing evidence primarily supports its research value as a potential adjuvant intervention target for sarcopenia.

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Research emphasis is on optimizing dosage and administration cycles, as well as exploring synergistic effects with other sarcopenia intervention drugs (such as creatine and androgens). The goal is to develop more effective and safer adjuvant intervention regimens, while also focusing on its potential to alleviate sarcopenia-related complications.

Research on Hexarelin as an Adjuvant Intervention for Osteoporosis

Core Regulatory Mechanisms 

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GH-IGF-1 Axis-Mediated Indirect Regulation

By promoting GH release, Hexarelin tablets indirectly increases IGF-1 levels. IGF-1 specifically acts on osteoblasts, promoting their proliferation, differentiation, and maturation while inhibiting apoptosis, thereby enhancing bone formation capacity. This is its core pathway for regulating bone metabolism and providing adjuvant intervention for osteoporosis, and it has been validated in various animal models.

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Direct Regulation of Bone Metabolism Cells

This drug can directly bind to GHSR-1a receptors on the surface of osteoblasts, promoting osteoblast synthesis of bone matrix (e.g., osteocalcin, alkaline phosphatase) and accelerating the bone mineralization process. Simultaneously, it can inhibit osteoclast activity, reducing osteoclast-mediated bone resorption. 

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Regulation of Bone Metabolism-Related Cytokines

By modulating relevant cytokines in the bone metabolism microenvironment, this medicine promotes the secretion of anti-inflammatory and pro-osteogenic factors while inhibiting the release of pro-resorption factors, further optimizing bone metabolic homeostasis. Additionally, its effects can be regulated by the estrogen environment, exhibiting site-specific effects in different skeletal regions.

Specific Adjuvant Intervention Effects

Improves Bone Structural Integrity: This medicine promotes the proliferation and thickening of trabecular bone, reduces trabecular bone breakage and thinning, enhances trabecular connectivity, and improves the microstructure of bone. This strengthens bone mechanical properties and reduces the risk of osteoporotic fractures (e.g., vertebral and hip fractures). It also helps mitigate vertebral bone loss trends induced by factors such as ovariectomy. 

 

Increases Bone Mineral Density (BMD) and Bone Mineral Content (BMC):By promoting bone formation and inhibiting bone resorption, it enhances BMD and BMC in key skeletal sites such as the lumbar spine and femur. This alleviates bone loss caused by osteoporosis. In a 60-day administration experiment on middle-aged female rats, it significantly increased lumbar spine BMC and bone area in intact rats, and increased femoral mid-shaft BMC and bone area in ovariectomized rats, validating its bone-enhancing effect.

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Delays Osteoporosis Progression:For various types of osteoporosis, including postmenopausal osteoporosis, age-related osteoporosis, and glucocorticoid-induced osteoporosis, it can modulate bone metabolic homeostasis to slow the rate of bone loss and alleviate disease progression. It shows particular potential for targeted intervention in estrogen deficiency-related osteoporosis. Furthermore, it can reduce levels of bone resorption markers (e.g., urinary deoxypyridinoline, lysylpyridinoline), supporting its inhibitory effect on bone resorption.

Current Research Status
 

 

Preclinical studies have confirmed that medicine has significant adjuvant intervention effects in various osteoporotic animal models (e.g., ovariectomized rats, aged rats, gonadectomized rats), effectively increasing BMD and improving bone structure. However, its osteogenic-promoting effect is dose-dependent and does not affect baseline levels of certain bone metabolism markers.
Currently in the early stages of clinical exploration, research primarily focuses on the safety, tolerability, and preliminary efficacy of medicine in osteoporosis patients. Key areas of investigation include administration routes (e.g., subcutaneous injection), dose optimization, and synergistic effects with conventional anti-osteoporotic drugs such as bisphosphonates and estrogen-based therapies. Attention is also given to its site-specific regulatory effects on different skeletal regions. Optimization of oral formulation bioavailability offers potential for clinical translation.
Existing research suggests that Hexarelin's regulatory effects on bone are related to the estrogen environment. Under different estrogen levels, its impact varies across skeletal sites such as the lumbar spine and femur, providing a reference direction for the development of targeted intervention strategies.

Specific effects of Hexarelin in different skeletal regions 

Hexarelin's regulation of bone metabolism depends on the homeostasis of the bone microenvironment. As a core regulatory factor in bone metabolism, estrogen influences its effects in three key dimensions:Receptor expression, cytokine balance, and skeletal site sensitivity.

Varied Sensitivity of Different Skeletal Sites to Estrogen:
Different skeletal sites, such as the lumbar spine and femur, exhibit distinct distributions and activities of osteoblasts and osteoclasts, as well as inherent differences in their responsiveness to estrogen (e.g., the lumbar spine is more sensitive to estrogen regulation). Since the efficacy of medicine relies on the responsiveness of local bone cells, its effects-modified by estrogen regulation-vary across skeletal sites, demonstrating site-specificity.

Estrogen Regulates GHSR-1a Receptor Expression:
The key mechanism by which this regulates bone metabolism is through binding to the GHSR-1a receptor on the surface of osteoblasts. Estrogen directly modulates the expression level of GHSR-1a on osteoblasts-under different estrogen conditions (e.g., normal physiological levels vs. estrogen deficiency), the quantity and activity of GHSR-1a on osteoblasts vary. This affects the binding efficiency of medicine to the receptor, leading to differences in its regulatory efficacy.

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Estrogen Alters the Bone Metabolism Cytokine Microenvironment:
This medicine exerts its effects partly by modulating cytokines involved in bone metabolism. However, estrogen itself regulates the secretion balance of these cytokines (pro-osteogenic and pro-resorptive factors).Under varying estrogen conditions, the types and concentrations of cytokines in the bone microenvironment differ, indirectly influencing Hexarelin's regulatory intensity on osteoblasts and osteoclasts, ultimately resulting in differentiated effects.

Development prospects

Hexarelin tablets is used for auxiliary intervention research in sarcopenia and osteoporosis, with its core relying on its regulation of the GH-IGF-1 axis and direct effects on muscle cells and bone metabolism cells. It achieves auxiliary intervention effects through "muscle enhancement, function preservation" and "promotion of bone formation, inhibition of bone resorption", both of which are mainly in preclinical research and early clinical exploration stage. At present, research has confirmed its effectiveness in animal models. Further optimization of the dosing regimen, validation of human clinical trial efficacy, and clarification of its long-term safety are needed to provide new research directions and potential targets for clinical intervention of sarcopenia and osteoporosis, without involving neuroprotective regulatory mechanisms and effects throughout the process.

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