Pinealon Tablet

Following stroke (including ischemic and hemorrhagic stroke), a cascade of ischemia and hypoxia occurs in brain tissue: a surge in oxidative stress in neurons of the ischemic penumbra, massive accumulation of reactive oxygen species (ROS), collapse of mitochondrial function, release of excitatory amino acid toxicity, and infiltration of inflammatory factors, ultimately leading to neuronal apoptosis and necrosis, resulting in neurological deficits such as motor, cognitive and speech impairments.

Preclinical studies: In a rat model of ischemic stroke, intervention with Pinealon (10 μg/kg, once daily for 7 consecutive days) increased the rat limb motor function score (Bederson score) by more than 40% compared with the control group, shortened the escape latency in the Morris water maze test by 35%, and significantly improved spatial memory ability. Meanwhile, pathological sections of brain tissue showed a 50% increase in the number of surviving neurons in the ischemic penumbra, enhanced synaptic density, and reduced glial scar hyperplasia.

Chronic cerebral circulatory insufficiency (CCCI) refers to persistent brain cell hypoxia and metabolic disorders caused by cerebral arteriosclerosis and insufficient cerebral perfusion. Its core pathological features include chronic hypoxic stress, energy depletion in brain cells, accumulated oxidative stress, and progressive decline in neurological function.

Inducing the expression of hypoxia-adaptive genes to improve cell survival under hypoxia

Pinealon tablet can activate hypoxia-inducible factor-1α (HIF-1α)-related pathways through epigenetic regulation, promoting the expression of hypoxia-adaptive genes such as vascular endothelial growth factor (VEGF) and glucose transporter 1 (GLUT-1). On the one hand, VEGF promotes cerebral microvascular neovascularization, improves microcirculation, and increases blood and oxygen supply to ischemic areas.

Optimizing mitochondrial energy metabolism to maintain cell function under hypoxia

During chronic ischemia, oxidative phosphorylation in brain cell mitochondria is blocked, leading to insufficient ATP production and neurological decline. Pinealon acts directly on mitochondria, enhancing the activity of mitochondrial respiratory chain complexes, improving ATP synthesis efficiency, reducing mitochondrial ROS production, and balancing energy supply and oxidative stress.

Animal experiments: In a rat model of chronic cerebral hypoperfusion, oral administration of Pinealon Tablet (100 ng/kg for 4 consecutive weeks) increased cerebral blood flow by 25%–30%, significantly elevated the activities of SOD and glutathione peroxidase in brain tissue, and reduced malondialdehyde (an oxidative damage marker) content by 40%. The Y-maze test showed significant improvements in working memory and spatial cognition in rats, with relief of symptoms such as dizziness and lethargy.

The core ingredient of the product, the EDR tripeptide (Glu-Asp-Arg), originates from long-term research by the team of Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology, Russia. In the 1980s, Khavinson's team proposed the "short peptide bioregulation" theory, holding that short peptides composed of 3–5 amino acids can penetrate the blood-brain barrier, regulate gene expression, and reverse neuronal senescence and damage.

In 1992, combining the triple requirements of neurotransmitter metabolism, energy supply and vascular regulation, the team screened amino acid combinations: glutamic acid regulates neural synapses, aspartic acid participates in energy metabolism, and arginine promotes cerebral blood flow. Through molecular simulation and in vitro experiments, the Glu-Asp-Arg tripeptide sequence was identified as the optimal structure and named Pinealon.

After the maturation of the synthesis process, the team shifted to the research and development of tablet formulations, optimizing oral absorption and stability: a precise microdose formulation and enteric coating technology were adopted to improve oral bioavailability and reduce gastrointestinal irritation.

Since 2001, the neuroprotective mechanisms of the product have been gradually elucidated, including antioxidant, anti-apoptotic, neurorepair-promoting and hypoxia adaptation-inducing effects. Numerous experiments have been conducted by global research institutions to verify its efficacy and safety in cerebrovascular diseases.