The research
The science behind every formulation.
Every compound Mazrek offers is backed by peer-reviewed research. Here's what the evidence shows.
50%
Decline in NAD+ levels between ages 40–60
15aa
Amino acids in BPC-157 — the simplest effective healing peptide
Semaglutide & Tirzepatide
GLP-1 Receptor Agonists
The mechanism
GLP-1 (glucagon-like peptide-1) is an incretin hormone secreted by intestinal L-cells in response to food intake. GLP-1 receptor agonists mimic this signal — activating receptors in the pancreas to stimulate insulin secretion, suppressing glucagon release, slowing gastric emptying, and signaling the hypothalamus to reduce appetite.
Body Protection Compound 157
BPC-157
Origin and structure
BPC-157 is a synthetic pentadecapeptide (15 amino acids) derived from a gastric protective protein first identified in human gastric juice. Its sequence — GEPPPGKPADDAGLV — is not found in any known natural peptide. It is remarkably stable and resists hydrolysis in acidic conditions.
Tissue repair and healing
Preclinical research demonstrates BPC-157 significantly accelerates healing of tendons, ligaments, muscle, and bone — in part by upregulating growth hormone receptor expression in fibroblasts, increasing collagen production, and modulating nitric oxide synthesis. Angiogenesis (new blood vessel formation) at wound sites is also enhanced.
Gut-brain axis
BPC-157 exhibits potent gastroprotective effects — healing gastric ulcers, restoring intestinal mucosal integrity, and counteracting NSAID-induced damage. Research also suggests modulation of dopaminergic and serotonergic systems, with potential neuroprotective and mood-stabilizing effects via the gut-brain axis.
Nicotinamide Adenine Dinucleotide
NAD+
Cellular biology
NAD+ is a coenzyme found in every living cell, required for over 500 enzymatic reactions. It exists in two interconvertible forms — NAD+ (oxidized) and NADH (reduced) — and serves as a critical electron carrier in the mitochondrial electron transport chain. Without adequate NAD+, cellular energy production fails.
Age-related decline and supplementation
NAD+ levels decline approximately 50% between ages 40 and 60, correlating with mitochondrial dysfunction, impaired DNA repair, and reduced sirtuin activity. Restoring NAD+ via IV or subcutaneous delivery bypasses oral bioavailability limitations, achieving significantly higher tissue concentrations than oral precursors like NMN or NR.
Longevity pathways
NAD+ directly activates sirtuins (SIRT1–SIRT7) — a family of longevity-linked deacylases that regulate circadian rhythms, cellular stress resistance, inflammation, and genome stability. PARP enzymes, which consume NAD+ during DNA repair, are also modulated — representing a direct link between NAD+ availability and genomic integrity over time.
Research & citations
References include the Bivas-Benita BPC-157 review (2003) and Yoshino et al. NAD+ metabolism (Cell Metabolism 2018). Individual patient outcomes vary. This content is educational and does not constitute medical advice. Consult a licensed provider before initiating any treatment.