The story of NMN

<LifeSpan-Why We Age, and Why We Don't Have To> by David A. Sinclair, Ph. D.


“Brilliant and enthralling.” —The Wall Street Journal"

ACCB contains biomaterials and plant-derived anti-oxidant concoction for skin and scalp tissue regeneration.

ACCB, Advanced cord blood-derived mesenchymal stem cell-derived cell booster for Skin & Hair.

Specially designed ACCB Skin and Hair are based on an advanced stem cell technology with biomimetic peptides, antioxidants, and nutriment concoction for restoring skin and hair cells that were affected by the aging process of internal and external factors.

Introduction-Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) 

Human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) have been suggested to promote tissue repair and have been used for tissue engineering in numerous studies. Not only can their multiple lineages replace aged or damaged cells, but their secretory factors can enhance tissue repair efficiency.

PATENT, W O 2017/123022

UCB-MSCs provide a high amount of growth factors

Stem cell-derived exosomes containing a high amount of growth factors

The protein expression level of EGF (epidermal growth factor), FGF (fibroblast growth factor), VEGF (vascular endothelial growth factor), TGF (transforming growth factor ), PDGF (platelet-derived growth factor), HGF (hepatocyte growth factor) was tested in the conditioned media of UCB, AD (adipose), and BM (bone marrow), Result shows the UCB-MSC exosome contains a higher level of growth factors compare with the exosome of AD and BM.


(β-nicotinamide mononucleotide) 



GROWTH FACTOR’s heat stability

ACCB SKIN & HAIR combine the protein heat stabilizing technology, which is a modified spherosome.

We combined modified spherosome technology in ACCB which is a kind of drug delivery system, and it was developed by modification of oleosome and cubosome for increasing heat-stability of proteins in ACCB.


Promotes ECMs gene expression


Suppresses melanogenesis



Experimental data is our own test
Experimental data is our own test

Use UCB-MSCs to determine the effects of both stem cells and their paracrine factors on reacquisition of hDPC (human dermal papilla cells) conduction ability to induce hair growth and to provide an effective therapeutic strategy for alopecia

UCB-MSCs promote hair follicle cycling, morphogenesis in vivo

hUCB-MSCs promoted the telogen-anagen transition, in particular, hair follicles that were treated with UCB-MSCs were transformed from the telogen phase to the early-and middle -anagen phases at 6 weeks.

NMN (β-nicotinamide mononucleotide) is a key of anti-aging.

As we age, metabolism—how our body converts food to energy—becomes less efficient as our cell’s powerhouses, the mitochondria, decline. As the result, the creation and utilization of cellular energy, cellular renewal, and the ability of our cells to respond to their changing environment are all impacted. 

"NMN targets metabolic aging by supplying declining metabolites and acting to preserve and help generate new mitochondria. 

Promotes healthy metabolic aging by:Increasing levels of the critical coenzyme NAD+ via the highly efficient precursor NMN,Protects and generates new mitochondria to support cellular energy."

Mitochondria play crucial roles in energy production, metabolism, apoptosis, and intracellular signaling.

Figure. Mitochondria can metabolize fuels, such as fatty acids, amino acids and pyruvate, derived from glucose.

During cellular stress or damage, mitochondria release a variety of signals to the cytosol and the nucleus to alert the cell of changes in mitochondrial function.


NAD+ Biosynthetic Pathways Decline With Age

FIGURE. Hypothetic molecule mechanisms of NAD+ decreased with aging. 

"Oxidative stress, DNA damage, and chronic inflammation are increased with aging, which results in accelerated NAD degradation via activation of CD38 and PARPs, or dysregulation of NAMPT.  Finally, decreased levels of NAD+ lead to various metabolic and age-associated diseases. "

Nicotinamide adenine dinucleotide (NAD) is a vital metabolic redox coenzyme found in eukaryotic cells and is necessary for over 500 enzymatic reactions.  In mammalian cells, NAD+ is synthesized predominantly through NMN, to replenish the consumption by NADase participating in physiologic processes including DNA repair, metabolism, and cell death.

NMN plays a crucial role in various biological processes, including metabolism, aging, cell death, DNA repair, and gene expression.

Oxidative DNA Damage Accumulates with Age 

DNA is vulnerable to oxidative damage which, if not repaired, can trigger mutagenesis and/or cell death via energy restriction. 

NAD+ related metabolism

Nicotinamide adenine dinucleotide (NAD+) levels in the cells deplete with aging and it is associated with downregulation of energy production in mitochondria, oxidative stress, DNA damage, and inflammatory conditions. 

However, NMN, as the precursor of NAD+, can slow down this process by elevating NAD+ levels in the body. 

Chronic inflammation and oxidative stress, which come along with aging, are the causes for reduction and inhibition of NAD+ biosynthesis. A number of in vivo studies have indicated affirmative results of therapeutic effects for various age-induced complications with NMN.


Depletion and reduction of NAD+ biosynthesis

Downregulation of energy production in mitochondria

Chronic inflammation and oxidative stress