Klotho-Derived Peptide 1

Klotho-Derived Peptide 1

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[ Sequence ] H-Phe-Gln-Gly-Thr-Phe-Pro-Asp-Gly-Phe-Leu-Trp-Ala-Val-Gly-Ser-Ala-Ala-Tyr-Gln-Thr-Glu-Gly-Gly-Trp-Gln-Gln-His-Gly-Lys-Gly-OH
[ Purity ] ≥95% 

[ Function ]
Renoprotective and anti-fibrotic effects

About Klotho-Derived Peptide 1
Klotho-Derived Peptide 1 may inhibit apoptosis and promote cell survival by binding to specific cell-surface receptors and activating intracellular signaling pathways, such as the PI3K-Akt pathway. In models of oxidative stress, the peptide upregulates the expression of antioxidant enzymes—such as superoxide dismutase (SOD) and catalase (CAT)—reduces intracellular reactive oxygen species (ROS) levels, and alleviates oxidative damage.
Some studies suggest that Klotho-Derived Peptide 1 may be involved in regulating glucose and lipid metabolism. In *in vitro* cell experiments and animal models, the peptide has been shown to enhance insulin sensitivity and promote glucose uptake and utilization; it also modulates the activity of enzymes related to lipid synthesis and breakdown, thereby influencing fat metabolism.
In the context of cardiovascular disease research, Klotho-Derived Peptide 1 improves cardiac function following myocardial infarction and reduces cardiomyocyte apoptosis and fibrosis. These effects may be mediated by the inhibition of the renin-angiotensin-aldosterone system (RAAS) and the suppression of inflammatory responses.
Research into neurological disorders indicates that Klotho-Derived Peptide 1 exhibits potential neuroprotective effects. In animal models of Parkinson's disease and Alzheimer's disease, administration of the peptide alleviates neuronal damage and improves cognitive and motor dysfunction. While these effects may be linked to the inhibition of neuroinflammation and the reduction of β-amyloid deposition and tau protein phosphorylation, the precise molecular mechanisms require further investigation.

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Daisy Chen is responsible for the global sales, service and channel expansion into the European market.