Agilon Health India Private Limited

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Nicotinamide adenine dinucleotide (NAD⁺) is a coenzyme for redox reactions, making it central to energy metabolism. NAD⁺ is also an essential cofactor for non-redox NAD⁺-dependent enzymes, including sirtuins, CD38 and poly(ADP-ribose) polymerases. NAD⁺ can directly and indirectly influence many key cellular functions, including metabolic pathways, DNA repair, chromatin remodelling, cellular senescence and immune cell function. These cellular processes and functions are critical for maintaining tissue and metabolic homeostasis and for healthy ageing. Remarkably, ageing is accompanied by a gradual decline in tissue and cellular NAD⁺ levels in multiple model organisms, including rodents and humans. This decline in NAD⁺ levels is linked causally to numerous ageing-associated diseases, including cognitive decline, cancer, metabolic disease, sarcopenia and frailty. Many of these ageing-associated diseases can be slowed down and even reversed by restoring NAD⁺ levels. Therefore, targeting NAD⁺ metabolism has emerged as a potential therapeutic approach to ameliorate ageing-related disease, and extend the human healthspan and lifespan. However, much remains to be learnt about how NAD⁺ influences human health and ageing biology. This includes a deeper understanding of the molecular mechanisms that regulate NAD⁺ levels, how to effectively restore NAD⁺ levels during ageing, whether doing so is safe and whether NAD⁺ repletion will have beneficial effects in ageing humans.

Nicotinamide adenine dinucleotide (NAD⁺) is an important coenzyme for redox reactions, making it central to energy metabolism. NAD⁺ is also an essential cofactor for non-redox NAD⁺-dependent enzymes, including sirtuins and poly(ADP-ribose) polymerases (PARPs).
NAD⁺ was first identified for its role in regulating metabolic rates in yeast extracts and later as the major hydride acceptor in redox reactions. This ability of NAD⁺ to accept a hydride ion, forming its reduced version, NADH, is critical for metabolic reactions of all living life forms and regulates the activity of dehydrogenases involved in multiple catabolic pathways, including glycolysis, glutaminolysis and fatty acid oxidation. The accepted electrons in these reactions are then donated to the electron transport chain to form ATP in eukaryotes. NAD⁺ can also be phosphorylated to form NADP⁺, which also acts as a hydride acceptor to form NADPH and is used in protection against oxidative stress and in anabolic pathways that require reducing power, such as fatty acid synthesis.
In addition to energy metabolism, NAD⁺ is used as a cofactor or substrate by hundreds of enzymes¹ and therefore has multiple roles in the regulation of cellular processes and cellular functions, many of which are still being investigated. Links between NAD⁺ levels and health were established almost a century ago. In 1937, Conrad Elvehjem discovered that the disease pellagra (characterized by dermatitis, diarrhoea and dementia) is caused by a dietary deficiency of niacin and resulted in low NAD⁺ and NADP⁺ levels. Recently, low NAD⁺ levels were linked to multiple disease states, including metabolic and neurodegenerative diseases, and lower NAD⁺ levels are now known to correlate with ageing in rodents and humans. As a result, there is renewed interest in understanding how NAD⁺ metabolism impacts the origin of diseases, particularly ageing-related diseases

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• Production Capacity: 1000
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Manufactured By	0.9 mg Xiapex Collagenase

The disease of Dupuytren is now being treated with Xiapex. Collagenase enzymes are combined in Xiapex to break down and digest the rope-like Dupuytren's cords' collagen. The injection weakens the cords to the point that they can occasionally break on their own, but more frequently they need to be straightened with a treatment I conduct at least a day following the injection

Additional Information:

• Production Capacity: 3000
• Delivery Time: 2-5 DAYS DELIVERY
• Packaging Details: SEALED