Hexarelin Tablets

After oral absorption, Hexarelin Tablets efficiently penetrate the blood‑brain barrier and specifically activate the widely expressed GHSR‑1a receptor in the central nervous system. Such activation directly initiates the PI3K/Akt core survival pathway, promoting Akt phosphorylation and thereby inhibiting the activity of the downstream pro‑apoptotic factor GSK‑3β, blocking the apoptotic cascade in neurons. Meanwhile, this pathway upregulates the expression of the anti‑apoptotic protein Bcl‑2 and downregulates mRNA and protein levels of pro‑apoptotic proteins Bax and Caspase‑3/7, inhibiting neuronal apoptosis at the molecular level and sustaining neuronal survival. Furthermore, GHSR‑1a activation stimulates pulsatile secretion of endogenous growth hormone, which crosses the blood‑brain barrier to act on neural tissue, enhancing neuronal metabolism and repair, thus indirectly strengthening neuroprotection.

Hexarelin specifically binds to the CD36 scavenger receptor on neuronal surfaces, with a binding site overlapping that of oxidized low‑density lipoprotein (oxLDL). It competitively blocks oxLDL‑CD36 binding and reduces oxLDL‑mediated oxidative damage to neurons. As oxidative stress is a key driver of neural injury, Hexarelin inhibits reactive oxygen species (ROS) production and reduces nitric oxide (NO) release via the CD36 pathway, while activating the antioxidant enzyme system to scavenge free radicals and alleviate toxicity from oxidative stressors such as H₂O₂. In addition, the CD36 pathway modulates the MAPK signaling pathway, suppressing abnormal phosphorylation of p38, ERK, and other MAPKs, reducing the release of inflammatory factors (e.g., TNF‑α, IL‑1β), alleviating inflammatory infiltration in neural tissue, and preserving homeostasis of the neural microenvironment.

Intracellular calcium overload is a critical event in ischemia‑ and oxidative stress‑induced injury. Hexarelin acts synergistically through both GHSR‑1a and CD36 pathways to inhibit the opening of voltage‑dependent calcium channels, reduce extracellular calcium influx, and promote endoplasmic reticulum calcium reuptake, maintaining intracellular calcium homeostasis and preventing calcium overload‑induced neuronal necrosis and apoptosis. Meanwhile, Hexarelin directly targets mitochondria, stabilizes mitochondrial membrane potential, inhibits mitochondrial permeability transition pore opening, reduces cytochrome C release, blocks the mitochondrial apoptotic pathway, and preserves mitochondrial energy metabolism to support neuronal repair.

Ischemic brain injury (e.g., stroke, neonatal hypoxic‑ischemic encephalopathy) is pathologically characterized by neuronal apoptosis, oxidative stress, and inflammation. Hexarelin Tablets demonstrate significant protective effects in these conditions. In rat models of neonatal hypoxic‑ischemic encephalopathy, oral Hexarelin reduces brain injury severity by 39%, markedly alleviates neuronal damage in the cerebral cortex, hippocampus, and thalamus, lowers Caspase‑3 activity, increases Akt phosphorylation, and inhibits neuronal apoptosis. In cerebral ischemia‑reperfusion models, Hexarelin reduces infarct volume and improves neurological deficit scores through antioxidant and anti‑inflammatory effects, with efficacy superior to some traditional neuroprotective agents. The oral formulation enables early and sustained intervention, enhancing clinical compliance.

Neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD) are closely associated with progressive neuronal apoptosis, accumulated oxidative stress, and neuroinflammation. In vitrostudies confirm that Hexarelin protects Neuro‑2A cells from Aβ oligomer‑ and α‑synuclein‑induced injury, inhibits tau hyperphosphorylation, and reduces neurofibrillary tangle formation. In AD animal models, Hexarelin improves hippocampal synaptic plasticity via the PI3K/Akt pathway, upregulates learning‑ and memory‑related proteins, and mitigates cognitive decline. In PD models, it protects dopaminergic neurons, reduces nigral dopaminergic loss, and improves motor dysfunction, providing a novel strategy for long‑term oral intervention in neurodegenerative diseases.

Peripheral nerve injury, spinal cord injury, diabetic peripheral neuropathy, and other conditions are often accompanied by persistent neuroinflammation and oxidative stress that impede neural repair. It inhibit excessive activation of microglia and astrocytes via CD36 and MAPK pathways, reduce pro‑inflammatory factor release, enhance antioxidant capacity, and alleviate oxidative damage to myelin sheaths and axons. In diabetic peripheral neuropathy models, oral Hexarelin improves nerve conduction velocity, repairs damaged nerve fibers, and relieves symptoms such as numbness and pain. In spinal cord injury models, it reduces inflammatory infiltration at the injury site, promotes neural stem cell proliferation and differentiation, and accelerates neurological recovery.

With the advantages of convenient oral administration, multi‑target protection, and high safety, Hexarelin Tablets show broad prospects in neuroprotection. Significant preclinical progress has been achieved in ischemic brain injury and neurodegenerative diseases. Future multi‑center, large‑sample clinical trials are needed to verify efficacy and safety in human stroke, AD, PD, and other disorders. Further formulation optimization (e.g., sustained‑release tablets) can prolong action duration and improve bioavailability, while combination with other neuroprotective agents may enhance synergistic effects. In‑depth exploration of Hexarelin's mechanisms in neural regeneration and neural stem cell regulation is expected to provide novel therapeutic strategies for severe neural injuries such as spinal cord injury and traumatic brain injury.