7 replies to this topic

[livingguy]

We know that Chromadex owns the patents for NR. Who owns the patents for NMN? 

[stefan_001]

Nobody holds the patents for NMN. Neither does Chromadex hold the patents for NR. Its not possible to IPR these body natural compounds. Chromadex does hold IPR for manufacturing of a stable NR salt.

[Turnbuckle]

Washington University in St. Louis holds use patents for both NR and NMN.

[Hebbeh]

In regards to NR, it is my understanding that chromadex didn't invent anything but merely licensed the manufacturing process from Dartmouth College whom developed and holds the patent for the process.

[LawrenceW]

Washington University in St. Louis holds use patents for both NR and NMN.

Could you provide us with any more detail as to what use they patented?

[Turnbuckle]

7,776,326

 

What is claimed is: 

 

1. A method of treating an axonopathy in a mammal in need thereof, the method comprising administering to the mammal an agent that acts by increasing sirtuin activity in diseased and/or injured neurons and supporting cells in an amount effective to decrease axonal degeneration. 

 

2. A method according to claim 1, wherein the agent acts by increasing SIRT1 activity. 

 

3. A method according to claim 1, wherein the agent is NAD, NADH, an intermediate of a de novo pathway for synthesizing NAD, an intermediate of a NAD salvage pathway, an intermediate of a nicotinamide riboside kinase pathway or a combination thereof. 

 

4. A method according to claim 1, wherein the agent is NAD, nicotinamide mononucleotide, nicotinic acid mononucleotide or nicotinamide riboside. 

 

5. A method according to claim 1, wherein the mammal is a human. 

 

6. A method in accordance with claim 4 wherein the agent is nicotinamide riboside.

 

 

 

and,

 

9,295,688

 

What is claimed is: 

 

1. A method of treating an axonopathy in a mammal in need thereof, the method comprising administering to the mammal a therapeutically effective amount of an agent that acts by increasing NAD activity in neurons and/or supporting cells wherein the agent is selected from the group consisting of NAD, nicotinamide mononucleotide, nicotinic acid mononucleotide and nicotinamide riboside. 

 

2. A method according to claim 1, wherein the mammal is a human. 

 

3. A method of treating an axonopathy in a human in need thereof, the method comprising administering to the human a therapeutically effective amount of an anent that acts by increasing NAD activity in neurons and/or supporting cells, wherein the agent is NAD. 

 

4. A method according to claim 2, wherein the agent is nicotinamide mononucleotide. 

 

5. A method according to claim 2, wherein the agent is nicotinic acid mononucleotide. 

 

6. A method according to claim 2, wherein the agent is nicotinamide riboside. 

 

7. A method according to claim 1, wherein the axonopathy is an axonopathy induced by a cytotoxic anticancer agent. 

 

8. A method according to claim 1, wherein the axonopathy is hereditary or congenital or associated with a neurodegenerative disease, a motor neuron disease, a neoplasia, an endocrine disorder, a metabolic disease, a nutritional deficiency, an autoimmune disease, a mechanical injury, a chemical or drug-induced injury, a thermal injury, a radiation injury, a nerve compression, a retinal or optic nerve disorder, mitochondrial dysfunction, progressive dementia, a demyelinating disease, ischemia and/or stroke, an infectious disease or an inflammatory disease. 

 

9. A method according to claim 8, wherein the retinal or optic nerve disorder is glaucoma, retinal ganglion degeneration, optic neuritis and/or degeneration, ischemic optic neuropathy, traumatic injury to the optic nerve, hereditary optic neuropathy, metabolic optic neuropathy, neuropathy due to a toxic agent, neuropathy caused by an adverse drug reaction, or neuropathy due to a vitamin deficiency. 

 

10. A method according to claim 8, wherein the axonopathy associated with mitochondrial dysfunction is an axonopathy resulting from oxidative damage, from mutations in mitochondrial proteins encoded in the mitochondrial genome, from mutations in mitochondrial proteins encoded in the nuclear genome, from exposure to toxins, or from the process of aging.

 

 

[livingguy]

Washington University in St. Louis holds use patents for both NR and NMN.

 

Chromadex has the license to produce NR commercially. So who has the license to produce NMN commercially? 

[Turnbuckle]

 

Washington University in St. Louis holds use patents for both NR and NMN.

 

Chromadex has the license to produce NR commercially. So who has the license to produce NMN commercially? 

 

 

 

I don't know. But a Sinclair application (filed a year ago as a division from an 2013 application) gives you an excellent clue of how to make it yourself--

 

1. A method for producing nicotinamide mononucleotide (NMN), comprising: providing an isolated cell that overexpresses a nicotinamide phosphoribosyltransferase (Nampt) enzyme; and culturing the isolated cell in the presence of nicotinamide (NAM). 

 

US patent application 20160287621

 

 

 

 

So you could produce this in your own body using NAM alone, as your body produces both Nampt (as well as ribose, not mentioned in the application). But adding ribose and stimulating Nampt will certainly help maximize endogenous NMN production. One Nampt stimulator is exercise. Endogenous production will be superior to taking NMN orally as NMN is broken down in the intestines (apart from small amounts absorbed gastrically).

Edited by Turnbuckle, 21 November 2017 - 11:05 AM.