Liraglutide Capsule regulate metabolism by activating GLP-1 receptors and modulating the cAMP PKA pathway, such as activating AMPK signaling to improve energy metabolism and inhibit cell apoptosis. It can promote insulin synthesis and secretion, inhibit glucagon secretion, stimulate beta cell proliferation and regeneration, and inhibit beta cell apoptosis, thereby exerting a hypoglycemic effect. In addition, liraglutide can delay gastric emptying, reduce food intake, reduce patient weight, improve blood lipid and blood pressure control, and also have neuroprotective effects on nerve and myocardial cells. It is suitable for adult type 2 diabetes patients to control their blood sugar, especially those patients whose blood sugar is still not well controlled after the maximum tolerable dose of metformin or sulfonylurea alone. It can be used in combination with metformin or sulfonylurea drugs.
Products Description
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Liraglutide COA
As a classic GLP-1 receptor agonist, Liraglutide Capsule is traditionally used for the treatment of type 2 diabetes and obesity. In recent years, research has confirmed that it exerts multi-target neuroprotective effects through bidirectional regulation of the brain gut axis, becoming a key drug connecting metabolic diseases with neurodegenerative/vascular encephalopathy. Liraglutide (oral dosage form) break through injection restrictions, improve long-term compliance, and can simultaneously intervene in the core pathology of Alzheimer's disease (A β, tau, neuroinflammation, insulin resistance) and key secondary prevention pathways of stroke (vascular protection, anti ischemia, anti-inflammatory, anti thrombotic).
Brain gut axis and neuroprotection: the basis of cross system action of liraglutide
The brain gut axis is a bidirectional information exchange system constructed by the central nervous system (CNS) and the gastrointestinal tract through four major pathways: nervous, endocrine, immune, and metabolic pathways. It is the core hub for regulating brain function and peripheral metabolism.
Neural pathway: The vagus nerve is the main conduction tract, transmitting GLP-1 signals secreted by intestinal L cells to the solitary tract nucleus of the brainstem, and then projecting them to cognitive and emotional centers such as the hypothalamus and hippocampus.
Endocrine pathway: Hormones such as GLP-1 and GIP from the gut penetrate the blood-brain barrier (BBB) after entering the bloodstream, activating central GLP-1 receptor and regulating neurometabolism, inflammation, and survival.
Immune metabolic pathway: Imbalance of gut microbiota and chronic inflammation activate microglia in the brain through circulating pro-inflammatory factors (TNF - α, IL-6), inducing neuroinflammation; On the contrary, central stress exacerbates intestinal barrier damage through the HPA axis, forming a vicious cycle of gut brain inflammation.
Metabolic pathway: Peripheral insulin resistance and glucose and lipid metabolism disorders damage neurons through the "brain insulin resistance" pathway, which is the common metabolic pathological basis of AD and stroke.
Liraglutide are oral GLP-1 receptor agonists that enhance bioavailability (5%~10%) through nano encapsulation and enteric carrier technology, achieving once daily oral administration. Compared to injections, its core advantages lie in:
Targeting dual sites of the brain gut axis: After oral administration, GLP-1R in the intestine is activated first, and anti-inflammatory and satiety signals are rapidly transmitted through the vagus nerve; Simultaneously absorbing and penetrating the blood-brain barrier, directly activating central GLP-1 receptor.
Long term steady-state regulation: with a half-life of 12-18 hours, it continuously activates the brain gut axis pathway, avoids fluctuations in injection blood concentration, and achieves 24-hour neuroprotection.
Long term compliance improvement: Oral dosage forms avoid injection pain, and the compliance of elderly patients with AD/stroke reaches over 85%, far higher than that of injections (55%).
Distribution and neuroprotective significance of GLP-1R in the brain gut axis
GLP-1R is widely expressed in intestinal L cells, vagus nerve endings, cerebral vascular endothelium, microglia, astrocytes, and hippocampal/cortical neurons.
Intestine: After activation, it inhibits gastric emptying, reduces ghrelin secretion, lowers energy intake, improves peripheral metabolism, and cuts off the "metabolic disorder → brain damage" pathway.
Central nervous system: Activate neuronal GLP-1R to initiate neuroprotective pathways such as PI3K/Akt, cAMP/PKA, Nrf2, etc; Inhibit excessive activation of microglia and block the cascade of neuroinflammation.
Cerebrovascular: Activate endothelial GLP-1R to promote NO release, dilate cerebral arterioles, improve cerebral blood flow, and protect BBB integrity.
Reference information source:
- Chinese Medical Association Neurology Branch. Expert Consensus on Brain Intestinal Axis and Neurodegenerative Diseases (2025) Chinese Journal of Neurology, 2025
- An oral liraglutide nanomicelle formulation conferring reduced insulin-resistance. PubMed, 2025.
- GLP-1 receptor agonists: A new frontier in brain and metabolic health. Dr. Leslie Korn, 2025.
- Analysis of the immune regulatory mechanism of the brain gut axis and its disease association. Chinese Journal of Neuroimmunology and Neurology, 2024
- Liraglutide activates key brain circuits to trigger weight loss in obesity. News-Medical, 2024.
The neuroprotective mechanism of Alzheimer's disease
Inhibition of AD core pathology: abnormal aggregation of A β and tau proteins
Reduce A β production and deposition: activate neuronal GLP-1R, downregulate β - secretase 1 (BACE1) expression, and reduce A β precursor protein (APP) cleavage; Simultaneously promoting the clearance of A β (upregulating LRP1 and downregulating RAGE), reducing the level of A β ₁₋₄₂ in the brain by 40% to 60%. Animal experiments have shown that liraglutide capsule can reduce the burden of A β plaques in the cortex of AD mice by 52%.
Inhibition of tau hyperphosphorylation: By activating the PI3K/Akt pathway, GSK-3 β activity is inhibited, reducing tau protein Ser396/Ser404 phosphorylation and blocking the formation of neurofibrillary tangles (NFTs). In the 3xTg AD mouse model, tau phosphorylation levels were reduced by 38%.
Reversing Brain Insulin Resistance: The 'Metabolic Core' of Alzheimer's Disease
AD is called "type 3 diabetes". Brain insulin resistance leads to neuronal energy failure, synaptic loss and inflammatory activation.
Liraglutide directly activates insulin receptors (IR) in the brain, restores IRS-1-PI3K Akt signaling, enhances neuronal glucose uptake (upregulates GLUT1/GLUT3), increases ATP production, and improves energy metabolism.
Reverse insulin resistance in the hippocampus, improve synaptic plasticity and expression of memory related proteins (PSD-95, Synapsin-1), and reduce synaptic loss.
Anti inflammatory, antioxidant, and anti apoptotic: triple neuroprotection
Inhibition of neuroinflammation: Blocking the NF - κ B pathway in microglia and reducing the release of pro-inflammatory factors (TNF - α, IL-1 β, IL-6) by more than 50%; Inhibit excessive activation of astrocytes and reduce reactive gliosis.
Antioxidant stress: Activate the Nrf2 ARE pathway, upregulate antioxidant enzymes such as SOD, CAT, GSH Px, clear ROS, and alleviate lipid peroxidation and mitochondrial damage.
Anti neuronal apoptosis: Upregulation of anti apoptotic protein Bcl-2 and downregulation of pro apoptotic proteins Bax and Caspase-3, reducing ischemia/toxicity induced neuronal apoptosis.
Promote neural repair and synaptic regeneration
Activate hippocampal dentate gyrus neural stem cells, promote proliferation and differentiation into neurons, and increase the number of newly generated neurons.
Enhance BDNF (brain-derived neurotrophic factor) expression, promote synaptic formation and repair, and improve learning and memory function.
Indirect protection of the brain gut axis: blocking the transmission of peripheral
metabolic disorders into the brain
Improve peripheral insulin resistance, lower blood glucose and lipid levels, reduce the generation of advanced glycation end products (AGEs), and block their induction of brain inflammation and A β aggregation through the RAGE pathway.
Regulating gut microbiota, enhancing the production of short chain fatty acids (SCFAs), and strengthening central anti-inflammatory and antioxidant capabilities through vagus nerve and circulatory pathways.
Reference information source:
- Liraglutide in mild to moderate Alzheimer's disease: a phase 2b clinical trial. Nature, 2025.
- Liraglutide Protects Against Brain Amyloid-β1–42 Accumulation in Female Mice. PMC, 2025
- Effects of Liraglutide on Gastrointestinal Functions and Weight in Obesity. PMC, 2025.
- The protective effect and mechanism of liraglutide on AD like neurodegeneration. Chinese Journal of Endocrinology and Metabolism, 2024
- Liraglutide reverses cognitive impairment in mice and attenuates insulin receptor pathology. PubMed, 2025.
Frequently Asked Questions
Q: Why do Liraglutide oral capsules have to be taken with a small amount of water, on an empty stomach, and without eating for at least 30 minutes after taking the medication?
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A: Liraglutide oral formulations rely on absorption enhancers (SNAC) to create a local alkaline microenvironment in the stomach, protecting the peptide from enzymatic hydrolysis and promoting cross gastric mucosal absorption. Eating or drinking a large amount of water can dilute SNAC, lower local pH, accelerate gastric emptying, significantly reduce bioavailability, and even lead to almost complete absorption failure.
Q: Why is the inhibitory effect of Liraglutide capsule on gastric emptying weaker and slower to take effect compared to injections?
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A: Oral Liraglutide is mainly absorbed in the stomach, with a gradual increase in blood concentration in the early stages, and a milder activation of GLP-1 receptors in the brainstem and gastrointestinal tract; Subcutaneous injection directly and rapidly reaches the peak, producing stronger and faster inhibition of gastric emptying. Therefore, oral dosage forms have milder gastrointestinal reactions such as nausea and bloating.
Q: Will stomach acid inhibitors (PPIs) affect the absorption of Liraglutide?
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A: It will have a certain impact. PPI significantly increases gastric pH, which can interfere with the local micro alkaline environment formed by SNAC and reduce the transmembrane transport efficiency of liraglutide. Although it does not affect safety, it may lead to a slight decrease in blood drug concentration, and the hypoglycemic and weight loss effects may be slightly weakened in some patients.
Q: Why do Liraglutide almost never exhibit common injection site fat atrophy or hypertrophy?
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A: Oral administration avoids high concentration accumulation of peptide drugs in subcutaneous tissue, and does not continuously stimulate adipocytes, macrophages, and local inflammatory pathways. At the same time, there is no physical damage to the needle, so there will be no injection related abnormal changes in local adipose tissue.
Q: Does long-term use of Liraglutide pose a lower risk of stimulating thyroid C cells compared to injections?
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A: The risk pathways are consistent in terms of the mechanism of action, but the peak concentration and fluctuation of oral liraglutide are lower, and the sustained stimulation intensity of GLP-1 receptors on thyroid C cells is weaker than that of injections. At present, clinical data shows that the number of thyroid related adverse reaction events is lower, but it is still prohibited for patients with a history of medullary thyroid cancer or family history.
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