This I learned too about one of the chemo treatments I was taking (Daratumumab), which targets CD38, a protein involved in the salvage pathway for creating NAD+. If you read below, it’s easy to see why we have to have the tryptophan and niacin for healing. It doesn’t mention Vitamin C but they just don’t know what Dmitry has discovered. Anyway, no wonder I feel so much better now that we have the CNT perfect triad for healing. I’m sure Dmitry has already shown this in dozens or hundreds of studies but I’m just figuring it all out, relative to what I was taking for cancer treatment and why I was never going to be healthy taking chemo instead of taking CNT.

(From AI)

CD38 has a complex relationship with the NAD+ salvage pathway; it is a NAD+-consuming enzyme that generates nicotinamide (NAM) which then enters the salvage pathway for recycling into NAD+. However, CD38 also directly interacts with nicotinamide mononucleotide (NMN), an intermediate of the salvage pathway, by mediating a base-exchange reaction that converts NMN into nicotinic acid mononucleotide (NaMN), a precursor for the Preiss-Handler pathway. This unexpected interaction creates a crossover point between the salvage and Preiss-Handler pathways.

CD38’s Main Role in NAD+ Metabolism

NAD+ Degradation:

CD38’s well-known function is to hydrolyze NAD+ into nicotinamide (NAM) and ADP-ribose (ADPR).

NAM in Salvage Pathway:

The NAM produced by CD38 is the primary substrate for the NAD+ salvage pathway, where it’s converted to NMN and then to NAD+.

CD38’s New Role: Interacting with the Salvage Pathway Intermediate

NMN Base Exchange: CD38 can also act on NMN, an amidated intermediate in the salvage pathway.

Crossover with Preiss-Handler Pathway: Through a base-exchange mechanism, CD38 can swap the nicotinamide moiety of NMN for nicotinic acid, converting NMN into NaMN.

Pathway Intersection: This action creates a crossover between the amidated salvage pathway and the deamidated Preiss-Handler pathway, which uses nicotinic acid as its precursor.

Implications of this Interaction

Complex Interplay:

This shows a more complex interconnection between the NAD+ biosynthesis pathways than previously understood.

NAD+ Homeostasis:

The interaction suggests that CD38 can influence the flow of intermediates between these two pathways, affecting overall NAD+ levels.

Disease Relevance:

CD38’s role in NAD+ metabolism and its complex interactions with the salvage pathway are relevant to age-related decline in NAD+ levels and the development of age-related diseases.