Cardax Pharmaceuticals. Focusing on the Source of Inflammation
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Compound Platform Rationale

Cardax Pharmaceuticals develops proprietary small molecule therapies for large unmet medical needs where oxidative stress and inflammation play important causative roles - including cardiovascular disease, hepatitis, macular degeneration, and many cancers.

Most anti-inflammatory drugs have significant issues, including long-term side effects that limit their utility. In contrast, the Company's proprietary, synthetic, natural compound derivatives have an outstanding safety profile, are orally bioavailable, and tissue selective.

Safety
Most drugs target highly specific biological enzymes or receptors such as COX-2, TNF-α, CCR2, etc. While these natural targets play a significant role in inflammation, they are also critical components of important biological pathways. With chronic use of these drugs, these pathways may not function normally - resulting in adverse events. Also, these treatments often negatively affect other crucial biological systems, creating additional side effects. The Company's proprietary compounds:

  • Localize in the plasma, mitochondrial, and nuclear membranes;
  • Scavenge or quench the unwanted initiators and perpetuators of inflammation - reactive oxygen and nitrogen species (ROS and RNS); and
  • Decrease infections in animals; with
  • No evidence of off-target effects (e.g. receptor or pathway).
As a result, the Company's compounds are inherently safer than most other anti-inflammatory treatments.

Mechanism of Action
Unlike other well-known anti-oxidants, the active metabolite of our lead proprietary compound spans plasma, mitochondrial, and nuclear membranes of cardiovascular tissue, stabilizing these membranes and reducing or preventing lipid peroxidation, including the oxidation of LDL (see Fig. 1). Its localization as well as its antioxidant and related anti-inflammatory effects reduce the oxidative stress that initiates and/or perpetuates the chronic and pathological activation of a number of inflammatory pathways, including NF-KB, JNK, and others. These data may help explain why other well-known anti-oxidants, such as beta-carotene, Vitamin C, and Vitamin E have not had clinical success.  
Fig. 1 McNulty, et.al. Biochip Biophys Acta. 2007;1768(1); 167-174


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