KPV peptide capsules are an oral supplement consisting of the tripeptide KPV (composed of lysine, proline, and valine) as the core ingredient, designed to improve health by regulating immune and inflammatory responses. As the C-terminal fragment of alpha melanocyte stimulating hormone (α - MSH), it naturally exists in the human body. However, after being extracted and concentrated into capsules, its biological activity is enhanced, enabling it to more efficiently exert anti-inflammatory, antibacterial, and immune regulatory effects. Usually taken on an empty stomach 1-2 times a day at a dose of 250-500 micrograms per dose to ensure optimal absorption. Research has shown that its oral form exerts a high concentration effect locally in the gastrointestinal tract, while supporting systemic anti-inflammatory needs through systemic circulation.
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KPV COA
Intestinal repair:
Reconstruction of mucosal barrier - multi-target mechanism and clinical translation of product
The integrity of the intestinal mucosal barrier depends on the dynamic balance between intestinal epithelial cells and the immune system. In inflammatory bowel disease (IBD), damage to the intestinal mucosal barrier leads to pathogens and their KPV peptide capsules (such as lipopolysaccharides, LPS) penetrating the intestinal wall, activating Toll like receptor 4 (TLR4) on the surface of intestinal epithelial cells, and triggering NF - κ B nuclear translocation through the myeloid differentiation factor 88 (MyD88) - dependent pathway, promoting the secretion of pro-inflammatory cytokines (such as IL-8, TNF - α). IL-8, as a neutrophil chemokine, can recruit a large number of neutrophils to infiltrate the intestinal mucosa, forming an "inflammatory cascade" that exacerbates intestinal wall edema, ulcers, and fibrosis.
The intervention mechanism of product:
By competitively binding to the LPS binding site of TLR4, the formation of TLR4/MyD88 complex is blocked, thereby inhibiting downstream NF - κ B activation. In the Crohn's disease (CD) model, enema (50 μ g/kg/day) can significantly reduce intestinal wall thickness (35% ↓) and mucosal ulcer area (62% ↓), and its effect is comparable to anti TNF - α monoclonal antibodies (such as Infliximab), but there is no immunogenic risk. In addition, it can also inhibit the formation of neutrophil extracellular traps (NETs) and reduce secondary damage to intestinal epithelium caused by oxidative stress.
Clinical evidence:
A randomized controlled trial (RCT) for patients with mild to moderate ulcerative colitis (UC) showed that after 8 weeks of treatment with this suppositories (100 mg/time, twice daily) combined with 5-aminosalicylic acid (5-ASA), the mucosal healing rate (Mayo endoscopic score ≤ 1) reached 85%, significantly higher than the single drug 5-ASA group (52%); And the one-year recurrence rate was reduced by 37% (12% vs. 19%) compared to the monotherapy group. Mechanism studies have confirmed that it can downregulate the expression of IL-6 and IL-17 in intestinal mucosa, while promoting Treg cell differentiation and reshaping intestinal immune tolerance.
2. Promote tight junction protein expression: enhance physical barrier function
The "physical gating" of the intestinal epithelial barrier is composed of tight junction (TJ) proteins such as claudin-1, occludin, and ZO-1, whose downregulation is a common feature of IBD and irritable bowel syndrome (IBS). The absence of TJ protein can lead to increased intestinal mucosal permeability ("intestinal leakage"), triggering systemic inflammatory reactions and metabolic disorders.
Intervention mechanism:
By activating the AMPK/SIRT1 pathway, the transcription and translation of TJ protein are promoted. In vitro experiments showed that after treating Caco-2 cells with KPV (10 μ M) for 24 hours, the transmembrane electrical resistance (TEER) value increased by 2.8 times, indicating a significant enhancement in intestinal epithelial barrier function; Meanwhile, luciferase reporter gene experiments showed that it can upregulate claudin-1 promoter activity by 1.9 times.
In the DSS induced colitis model, oral administration (10 mg/kg/day) restored the continuous distribution of ZO-1 in the intestinal mucosa and reduced intestinal leakage of fluorescein isothiocyanate (FITC) - glucan (53% ↓).
Clinical evidence:
An open label trial targeting patients with IBS-D (Diarrhea predominant IBS) showed that after 4 weeks of oral treatment (100 mg/day), the frequency of abdominal pain decreased from 5.2 times per week to 2.1 times per week (59% ↓), and the stool hardness (Bristol score) improved from type 6 (pasty stool) to type 4 (soft stool). Mechanism studies suggest that KPV peptide capsules can reduce the release of 5-hydroxytryptamine (5-HT) from intestinal chromaffin cells (EC), thereby reducing visceral hypersensitivity; Meanwhile, by upregulating the expression of mucin-2 (MUC2) in the intestinal mucosa, the thickness of the mucus layer was enhanced (22% ↑).
3. Regulating gut microbiota: Inhibiting pathogenic bacteria and promoting probiotic colonization
Dysbiosis of gut microbiota is the core cause of IBD and antibiotic associated diarrhea (AAD). Pathogenic bacteria (such as Escherichia coli and Salmonella) bind to intestinal epithelial cells through adhesins (such as FimH) to form biofilms and evade host immune clearance; Probiotics, such as Bifidobacterium and Lactobacillus, maintain microbial balance by producing short chain fatty acids (SCFAs) and antimicrobial peptides, such as bacteriocins.
Intervention mechanism:
Reshaping the microbial community structure through the following three aspects:
Inhibition of pathogen adhesion: can competitively bind to the mannose binding site of FimH, blocking the adhesion of Escherichia coli to intestinal epithelium (in vitro experiments showed a 71% reduction in adhesion rate);
Destruction of biofilm: By producing reactive oxygen species (ROS) and downregulating the expression of biofilm related genes (such as csgD), the Salmonella biofilm is disrupted (biofilm thickness is reduced by 68%);
Promoting the proliferation of probiotics: can upregulate the F6PPK enzyme activity of bifidobacteria, enhancing their tolerance to low pH environments; At the same time, by activating GPR41/GPR43 receptors, it promotes the secretion of IgA (32% ↑) by intestinal epithelial cells, providing an anchoring point for probiotics to colonize.
In the AAD model, oral administration (5 mg/kg/day) restored the Shannon index of gut microbiota diversity to a healthy level (increasing from 2.1 to 3.8), while reducing the expression of Clostridium difficile toxin A (83% ↓).
Clinical evidence:
A randomized controlled trial (RCT) targeting AAD patients showed that after 5 days of treatment with a combination of probiotics (Bifidobacterium and Lactobacillus), the duration of diarrhea was shortened by 2.1 days (3.2 days vs. 5.3 days) compared to the group treated with probiotics alone, and the relative abundance of butyrate producing bacteria (such as Rossella) in the gut microbiota increased by 2.4 times.
Neuroprotection:
Breaking through the blood-brain barrier - Innovative anti-inflammatory, antioxidant, and delivery methods
The core mechanism of cerebral ischemia-reperfusion (I/R) injury is overactivation of microglia and activation of NLRP3 inflammasome, leading to the massive release of pro-inflammatory cytokines such as IL-1 β and IL-18, causing neuronal apoptosis and expansion of cerebral infarction volume.
Intervention mechanism:
It exerts neuroprotective effects through the following pathways:
Inhibition of M1 polarization in microglia: can block NF - κ B nuclear translocation, reduce the expression of iNOS and COX-2, thereby reducing the production of reactive oxygen species (ROS) in NO and PGE2;
Inhibition of NLRP3 inflammasome assembly: By upregulating the Nrf2/HO-1 pathway, the nitration modification of NLRP3 protein (a key activation step) is reduced, thereby inhibiting caspase-1 cleavage and IL-1 β maturation.
In the model of middle cerebral artery occlusion (MCAO), intravenous injection (10 mg/kg) can reduce the volume of cerebral infarction by 65% (from 320 mm ³ to 112 mm ³), and at the same time, the neurological deficit score (mNSS) can be reduced by 65% (from 12 points to 4 points), which is better than the traditional neuroprotective agent edaravone (38% ↓).
The common pathological features of Parkinson's disease (PD) and Alzheimer's disease (AD) are abnormal protein aggregation (such as alpha synuclein, A β) and oxidative stress damage. It enhances cellular antioxidant capacity by activating the Nrf2/HO-1 pathway, while promoting the clearance of abnormal proteins by proteasomes and autophagosomes.
Intervention mechanism:
In the PD model, KPV (5 mg/kg/day, intraperitoneal injection) can:
Upregulation of HO-1 expression in the substantia nigra by 2.3 times and reduction of α - synuclein oligomer formation (61% ↓);
Activate PINK1/Parkin mediated mitochondrial autophagy and clear damaged mitochondria (38% ↓);
Promote the secretion of neurotrophic factor (BDNF) and support the survival of dopaminergic neurons (with a 40% increase in survival rate).
In the AD model, combined focused ultrasound (FUS) delivery can reduce A β plaques in the hippocampus by 58% (from 12.4/mm ² to 5.2/mm ²), while improving spatial memory ability in the Morris water maze test (shortening escape latency by 42%).
The mechanism of neuropathic pain (such as pain after sciatic nerve ligation) involves excessive excitation of spinal dorsal horn neurons and activation of glial cells. Reduce pain signal transmission by regulating ion channels and neurotransmitter release.
The intervention mechanism of KPV peptide capsules:
In the sciatic nerve ligation model, this product (2 mg/kg, intrathecal injection) can:
Inhibiting the expression of α 2 δ -1 subunit in voltage-gated calcium channels (VGCC) and reducing glutamate release (53% ↓);
Downregulate P2X4 receptor expression and block ATP induced glial cell activation (IL-1 β secretion reduced by 71%);
Restore GABAergic interneuron function and enhance inhibitory transmission (GABA levels increase by 2.1 times).
Behavioral tests have shown that it can increase the mechanical pain threshold by 3.2 times (from 2.1 g to 6.8 g), and the effect lasts for 24 hours, which is better than gabapentin (2.1 times).
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