Description

Product Description

KRES peptide is a synthetic apolipoprotein-mimetic peptide composed of four amino acid residues (Lys-Arg-Glu-Ser). Despite its short sequence, KRES peptide demonstrates remarkable biological activity, mimicking certain structural and functional features of apolipoprotein A-I (apoA-I)—the major protein component of high-density lipoprotein (HDL).

Through specific interactions with phospholipids and lipoprotein particles, KRES peptide modulates oxidative lipid metabolism and enhances antioxidant defenses. It effectively reduces lipid hydroperoxide (LOOH) accumulation, which is a key contributor to oxidative stress and atherosclerosis progression.

Unlike many bioactive peptides that require parenteral administration, KRES peptide is orally active, making it particularly attractive for translational studies targeting lipid metabolism, vascular inflammation, and cardiovascular protection.

Scientific Background

Apolipoproteins play central roles in lipid transport, metabolism, and antioxidative regulation. ApoA-I, the principal component of HDL, exerts anti-atherogenic effects by promoting cholesterol efflux, inhibiting oxidation of low-density lipoproteins (LDL), and activating HDL-associated enzymes such as paraoxonase-1 (PON1) and lecithin-cholesterol acyltransferase (LCAT).

KRES peptide, designed to emulate the amphipathic α-helical segments of apoA-I, binds lipid molecules and exerts HDL-like antioxidant and anti-inflammatory activities. Its structure enables interaction with lipid bilayers and facilitates the neutralization of reactive oxygen species (ROS) generated during lipid peroxidation.

Product Specifications

Mechanism of Action

The KRES peptide exerts its biological effects primarily through lipid–protein interactions and activation of HDL-associated antioxidant pathways:

1. Lipid Binding and Membrane Interaction
   The amphipathic structure of KRES allows it to integrate with lipid bilayers and lipoprotein particles, mimicking apoA-I’s lipid-binding function.

2. Reduction of Lipid Hydroperoxides (LOOH)
   KRES peptide scavenges peroxyl radicals and reduces existing lipid hydroperoxides, preventing the propagation of lipid oxidation and oxidative stress.

3. Activation of HDL-Associated Antioxidant Enzymes
   The peptide enhances the activity of paraoxonase-1 (PON1) and LCAT, both key enzymes in HDL-mediated lipid detoxification.

4. Anti-inflammatory Effects
   By limiting oxidative lipid damage, KRES peptide downregulates vascular adhesion molecules (VCAM-1, ICAM-1) and inflammatory cytokines (TNF-α, IL-6).

5. Anti-atherogenic Action
   Through its combined antioxidant and anti-inflammatory properties, KRES peptide prevents endothelial dysfunction, lipid deposition, and plaque progression.

6. Oral Bioavailability
   Unlike most peptides degraded by gastrointestinal enzymes, KRES peptide remains partially intact after oral administration, retaining biological activity—a rare and valuable feature in peptide therapeutics.

   

Side Effects

KRES peptide has shown an excellent safety profile in preclinical studies. Nonetheless, potential laboratory observations include:

• Mild Gastrointestinal Disturbances — Due to oral bioavailability testing.

• Transient Blood Pressure Changes — Resulting from vasodilatory HDL activation.

• Minor Metabolic Adjustments — Modulation of lipid and glucose metabolism in prolonged exposure.

• Allergic Reactions — Rare peptide hypersensitivity events in sensitive animal models.

All experimental use should follow standard laboratory safety and peptide-handling procedures.

Disclaimer

For research use only. Not intended for human or veterinary use, diagnosis, or therapeutic applications.

Keywords

KRES peptide, apolipoprotein peptide, HDL mimetic, antioxidant peptide, lipid hydroperoxide reduction, paraoxonase activator, anti-atherogenic peptide, cardiovascular research peptide, orally active peptide, HDL antioxidant modulator.

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