Metabolic Bundle

Description

Product Details:

The Advanced Metabolic & Mitochondrial Optimization System is a multi-vector research platform designed to investigate the complete hierarchy of metabolic regulation. Unlike single-agent protocols that target only glycemic control, this stack simultaneously modulates systemic incretin signaling, cellular processes, and reduces mitochondrial ROS while providing holistic metabolic support.

The Metabolic Stack is designed to impact three critical pathways crucial for supporting Metabolic Health:

• Systemic Input Control: Regulate satiety and insulin sensitivity via incretin mimetics
• Cellular Energy: Upregulates the NAD+ Salvage pathways and inhibition of lipogenesis
• Mitochondrial Biogenesis: Direct activation of AMPK and ERRα pathways to simulate exercise-induced adaptation

The Metabolic Stack contains 2 phases.

Phase 1:

The first phase starts with a GLP-1 agonist – either a dual or triple-agonist incretin mimetic.  This supports appetite regulation and improves insulin sensitivity in adipose tissue while also reducing pro-inflammatory cytokines.  If a triple-agonist incretin mimetic is used, additional energy expenditure and hepatic lipid oxidation occurs via the engagement of the glucagon receptor.

Glutathione (GSH), known as the master antioxidant, is foundational in maintaining mitochondrial integrity during prolonged periods of upgraded beta-oxidation.  GSH is known to neutralize free radicals known as Reactive Oxygen Species (ROS) generated as a byproduct of the Electron Transport Chain (ETC) which can damage the inner mitochondrial membrane. (source)

5-Amino-1MQ (5AMQ) is a selective, membrane-permeable inhibitor of NNMT (Nicotinamide N-methyltransferase) that inhibits the NAD+ salvage pathway.  By inhibiting NNMT, 5AMQ prevents the methylation of NAM (Nicotinamide, B3) thereby increasing the intracellular pool of NAD+ available for sirtuin activation and metabolic processes. (source)

Phase 2:

The second phase continues with a GLP-1 agonist, stops GSH and 5AMQ applications, and starts the process of improving metabolic health by optimizing mitochondrial function via enhanced AMPK phosphorylation, the addition of a strong ERR agonist, and by increasing NAD+ directly using a proprietary, sublingual delivery method.

MOTS-c regulates nuclear gene expression and the folate cycle, promoting glocose disposal and free fatty acid oxidation.  Its primary MOA involves the phosphorylation of AMPK (Adenosine Monophosphate-Activated Protein Kinase), enhances insulin sensitivity, and promotes metabolic homeostasis. (source)

SLU-PP-332 is a small molecule agonist of the orphaned ERR receptors that acts as an exercise mimetic; showing greater affinity on the ERR-α compared to the ERR-β and ERR-γ.  Unlike traditional metabolic agents that target the PPAR family, SLU-PP-332 promotes mitochondrial biogenesis via the ERR-α transcription factors that remodel skeletal muscle fibers towards an oxidative (Type I) phenotype. (source)

NAD+ is a critical coenzyme that serves as the primary electron transporter for the mitochondrial electron transport chain to generate ATP.  It functions as the obligatory substrate for the Sirtuin family (SIRT1-7) of deacetylases, regulating signaling pathways that control DNA repair, inflammation, and circadian rhythm.  By optimizing the intracellular NAD+/NADH redox ratio, NAD+ drives efficient metabolic processes and supports the demands of mitochondrial biogenesis.  A proprietary CPP delivery mechanism enhances bioavailability via the oral mucosal membrane. (source)

Phase 3 (Optional):

An optional 3rd phase can be included in the metabolic stack by incorporating a clinically significant addition of L-Carnitine; this ranges from 600mg (intramuscular or subcutaneous) to 3000mg (oral) as well as another cycle of GSH.