OXIPASSIVE®

METABOLIC PCOS

Glutathione: The Missing Link in Metabolic PCOS

Restoring endogenous glutathione to rebalance redox homeostasis, improve metabolic function and support ovarian physiology.

Illustrated ovary with multiple follicles and a fallopian tube

Hyperandrogenism
Excess androgen activity disrupting systemic cycle control
Insulin Resistance
Impaired peripheral glucose transport and metabolic balance
Oxidative Stress
Sustained redox disruption resulting in follicular damage

Glutathione: The Body's Master Antioxidant - And the Missing Link in Metabolic PCOS

When endogenous glutathione drops, the body loses its primary defense against oxidative stress. The result is a cascade of metabolic dysregulation that can drive insulin resistance, hyperandrogenism, and ovulatory dysfunction.

1
NF-κB Activation
2
Chronic Inflammation
3
Oxidative Stress
4
Insulin Resistance
5
Hyperandrogenism

6
GSH Depletion
7
Mitochondrial Dysfunction
8
Ovulatory Dysfunction

Oxipassive® Dual-Precursor Strategy

N-Acetylcysteine
+
Glycine
Glutathione (GSH)
Cellular Redox Balance

Pathology & Clinical Management

Understanding the multi-faceted cellular profile of Metabolic PCOS.

Patient Profile

Hyperandrogenism
Excess androgen activity
Insulin Resistance
Impaired glucose metabolism
Low-grade Inflammation
Chronic inflammatory state
Oxidative Stress
Increased reactive oxygen species
Ovulatory Dysfunction
Impaired follicular development

Clinical Dose

Oxipassive®

One capsule twice daily for 3–6 months.

ADJUVANT CLINICAL NOTE:

Adjuvant therapy designed specifically for mitigating redox stressors in metabolic phenotypes of PCOS.

Clinical Challenge

Metabolic PCOS is driven by a self-perpetuating cycle of hormonal, metabolic, and inflammatory disturbances that disrupt ovarian function.

Vicious cycle linking hyperandrogenism, insulin resistance, inflammation and oxidative stress

This vicious cycle sustains oxidative stress and glutathione depletion, leading to mitochondrial dysfunction and impaired ovulation.

The Science of Dual-Precursor Supplementation

How restoring endogenous Glutathione addresses key intracellular pathologies.

Why Oxidative Stress Matters

ROS — Damages cells and DNA
NF-κB — Activates inflammatory pathways
Disrupts insulin signaling and glucose metabolism
Impairs mitochondrial function and oocyte quality

Why NAC?

Precursor for glutathione synthesis
Reduces oxidative stress
Modulates NF-κB activation
Supports insulin signaling
Protects ovarian cells

Why Glycine?

Essential substrate for glutathione synthesis
Supports mitochondrial function
Anti-inflammatory properties
Supports metabolic homeostasis

Why Dual-Precursor?

Supplies both precursor (NAC) and substrate (Glycine)
Enhances endogenous glutathione synthesis
Improves redox balance and mitochondrial function

Expected Clinical Benefits

Metabolic Function

Supports Insulin Sensitivity
Enhances peripheral glucose utilization
Supports Mitochondrial Function
Optimizes cellular energy production

Redox Homeostasis

Restores Glutathione
Replenishes depleted intracellular GSH pool
Reduces Oxidative Stress
Neutralizes reactive oxygen species
Supports Inflammatory Balance
Down-regulates pro-inflammatory cytokines

Ovarian Function

Supports Ovarian Health
Protects follicular microenvironment
Supports Ovulatory Function
Regulates natural cellular cycles
Addresses Oxidative Stress in Metabolic PCOS
Optimizes oocyte development environment