Prednosti NMNH
NMNH: 1. "Bonzyme" Celotna encimska metoda, okolju prijazna, brez škodljivih ostankov topil za proizvodnjo praška. 2. Bontac je prva proizvodnja na svetu, ki proizvaja prah NMNH na ravni visoke čistosti in stabilnosti. 3. Ekskluzivna sedemstopenjska tehnologija čiščenja "Bonpure", visoka čistost (do 99%) in stabilnost proizvodnje prahu NMNH 4. Tovarne v lastni lasti in pridobili številne mednarodne certifikate za zagotovitev visoke kakovosti in stabilne oskrbe z izdelki iz prahu NMNH 5. Zagotovite storitev prilagajanja rešitve izdelka na enem mestu
Prednosti NADH
NADH: 1. Celotna encimska metoda Bonzyme, okolju prijazna, brez škodljivih ostankov topil 2. Ekskluzivna tehnologija čiščenja v sedmih korakih Bonpure, čistost višja od 98 % 3. Posebna patentirana procesna kristalna oblika, večja stabilnost 4. Pridobil številne mednarodne certifikate za zagotovitev visoke kakovosti 5. 8 domačih in tujih patentov NADH, ki vodijo industrijo 6. Zagotovite storitev prilagajanja rešitve izdelka na enem mestu
Prednosti NAD
NAD: 1. "Bonzyme" Celotna encimska metoda, okolju prijazna, brez škodljivih ostankov topil 2. Stabilen dobavitelj 1000+ podjetij po vsem svetu 3. Edinstvena "Bonpure" sedemstopenjska tehnologija čiščenja, višja vsebnost izdelka in višja stopnja konverzije 4. Tehnologija liofilizacije za zagotovitev stabilne kakovosti izdelka 5. Edinstvena kristalna tehnologija, večja topnost izdelka 6. Tovarne v lastni lasti in pridobljene številne mednarodne certifikate za zagotavljanje visoke kakovosti in stabilne oskrbe z izdelki
Prednosti MNM
NMN: 1. "Bonzyme"Celotna encimska metoda, okolju prijazna, brez škodljivih ostankov topil 2. Ekskluzivna sedemstopenjska tehnologija čiščenja "Bonpure", visoka čistost (do 99,9%) in stabilnost 3. Vodilna industrijska tehnologija: 15 domačih in mednarodnih patentov NMN 4. Tovarne v lastni lasti in pridobljene številne mednarodne certifikate za zagotavljanje visoke kakovosti in stabilne dobave izdelkov 5. Številne študije in vivo kažejo, da je zdravilo Bontac NMN varno in učinkovito 6. Zagotovite storitev prilagajanja rešitve izdelka na enem mestu 7. Dobavitelj surovin NMN slavne ekipe Davida Sinclaira z univerze Harvard
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Bontac Bio-Engineering (Shenzhen) Co., Ltd. (hereafter referred to as BONTAC) is a high-tech enterprise established in July 2012. BONTAC integrates R&D, production and sales, with enzyme catalysis technology as the core and coenzyme and natural products as main products. There are six major series of products in BONTAC, involving coenzymes, natural products, sugar substitutes, cosmetics, dietary supplements and medical intermediates.
As the leader of the global NMN industry, BONTAC has the first whole-enzyme catalysis technology in China. Our coenzyme products are widely used in health industry, medical & beauty, green agriculture, biomedicine and other fields. BONTAC adheres to independent innovation, with more than 170 patentov za izume. Different from the traditional chemical synthesis and fermentation industry, BONTAC has advantages of green low-carbon and high-value-added biosynthesis technology. What’s more, BONTAC has established the first coenzyme engineering technology research center at the provincial level in China which also is the sole in Guangdong Province.
In the future, BONTAC will focus on its advantages of green, low-carbon and high-value-added biosynthesis technology, and build ecological relationship with academia as well as upstream/downstream partners, continuously leading the synthetic biological industry and creating a better life for human beings.
Lastnosti in prednosti izdelka BONTAC NAD
1 、 Encimska metoda, okolju prijazen, brez škodljivih ostankov topil proizvodni prašek
2, Visoka čistost (do 99%) in stabilnost proizvodnje prahu NAD
3 、 Tovarne v lastni lasti in pridobili številne mednarodne certifikate za zagotovitev visoke kakovosti in stabilne dobave izdelkov iz prahu NAD
4、Več študij in vivo kaže, da je prašek Bontac NAD varen in učinkovit
5 、 Zagotovite storitev prilagajanja rešitev izdelka na enem mestu
Način izdelave prahu NAD
The preparation methods of NAD powder are mainly divided into chemical synthesis method and biocatalytic method, among which biocatalytic method includes biological fermentation method and enzyme catalysis method. Enzyme catalysis method has gradually become the mainstream direction because of its advantages of green, environmental protection and pollution-free. And then the purity of NAD powder will reach 99% after the procedure of further purifying.
Učinkovitost praška NAD v zdravju
Molecules that can be taken in supplement form to increase NAD levels in the body are referred to by some as “NAD boosters.” Studies conducted over the past six decades suggest that the following are some of the many benefits associated with taking an NAD supplement:
Lahko pomaga obnoviti funkcijo mitohondrijev
Helps Repair Blood Vessels —A 2018 mice study found that supplementation could aid in repair and growth of aged blood vessels. There’s also some evidence it can help manage heart disease risk factors like high blood pressure and high cholesterol.
May Improve Muscle Function — One animal study conducted in 2016 found that degenerative muscles had improved muscle function when supplemented with NAD+ precursors.
Potentially Helps Repair Cells and Damaged DNA — Some studies have found evidence that NAD+ precursor supplementation leads to an increase in DNA damage repair. NAD+ is broken down into two component parts, nicotinamide and ADP-ribose, which combine with proteins to repair cells.
May Help Improve Cognitive Function — Several studies conducted on mice have found that mice treated with NAD+ precursors experienced improvements in cognitive function, learning and memory. Findings have led researchers to believe that NAD supplement may help protect against cognitive decline/Alzheimer’s disease.
May Help Prevent Age-Related Weight Gain — A 2012 study showed that when mice fed a high-fat diet were given an NAD supplement, they gained 60 percent less weight than they did on the same diets without the supplement. One reason this may be true is that nicotinamide adenine dinucleotide helps regulate production of stress- and appetite-related hormones, thanks to its effects on circadian rhythms.
Predhodne sestavine so molekule, ki se uporabljajo v kemijskih reakcijah v telesu za ustvarjanje drugih spojin. Obstajajo številni predhodniki NAD +, ki povzročijo višje ravni, ko jih zaužijete dovolj.
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Nikotinamid adenin dinukleotid (NAD) ima več bistvenih vlog v presnovi. Deluje kot koencim v redoks reakcijah, kot donator ADP-riboznih delov v ADP-riboziranih reakcijah, kot predhodnik druge molekule sporočila ciklične ADP-riboze, kot tudi kot substrat za bakterijske DNA ligaze in skupino encimov, imenovanih sirtuini, ki uporabljajo NAD + za odstranjevanje acetilnih skupin iz beljakovin. Poleg teh presnovnih funkcij se NAD + pojavlja kot adeninski nukleotid, ki se lahko spontano in z reguliranimi mehanizmi sprosti iz celic in ima zato lahko pomembne zunajcelične vloge.
Najprej preglejte tovarno. Po nekaj pregledih je NAD spremljal, da potrošniki neposredno soočijo več pozornosti izgradnji blagovne znamke. Zato je za dobro blagovno znamko najpomembnejša kakovost, prva stvar za nadzor kakovosti surovin pa je pregled tovarne. Podjetje Bontac dejansko proizvaja visoko kakovosten NAD prah s katerijami SGS. Drugič, preizkušena je čistost. Čistost je eden najpomembnejših parametrov prahu NAD. Če ni mogoče zagotoviti visoke čistosti NAD, bodo preostale snovi verjetno presegle ustrezne standarde. Kot je razvidno iz priloženih certifikatov, prah NAD, ki ga proizvaja družba Bontac, doseže čistost 99,9 %. Končno je za dokazovanje potreben strokovni testni spekter. Običajne metode za določanje strukture organske spojine vključujejo jedrsko magnetno resonančno spektroskopijo (NMR) in masno spektrometrijo visoke ločljivosti (HRMS). Običajno se lahko z analizo teh dveh spektrov predhodno določi struktura spojine.
The difference all comes down to the charge of these coenzymes. NAD+ is written with a superscript + sign because of the positive charge on one of its nitrogen atoms. It is the oxidized form of NAD. It’s considered “an oxidizing agent” because it accepts electrons from other molecules.
Čeprav se kemično razlikujejo, se ti izrazi večinoma uporabljajo zamenljivo, ko razpravljamo o njihovih koristih za zdravje. Drug izraz, na katerega lahko naletite, je NADH, ki pomeni nikotinamid adenin dinukleotid (NAD) + vodik (H). To se večinoma uporablja tudi zamenljivo z NAD +. Oba sta nikotinamid adenin dinukleotidi, ki delujeta kot hidridni donorji ali akceptorji hidridov. Razlika med tema dvema je v tem, da NADH postane NAD +, potem ko podari elektron drugi molekuli.
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Najnovejše raziskave dokazujejo: Koencim NAD + lahko poveča tumorsko imunost! Strokovni komentar Kitajske akademije znanosti
On August 10, 2021, researchers from Shanghai University of Science and Technology published an article titled NAD+ supplement potentiates tumor killing function by rescuing defective TUBBY-mediated NAMPT transcription in tumor infiltrated T cells in Cell Reports, revealing that NAD+ in supplemented during CAR-T therapy and immune checkpoint inhibitor therapy, it can improve the anti-tumor activity of T. At present, the supplementary precursor of NAD+, as a nutritional product,has been verified for human consumption safety.This achievement provides a simply and feasible new method for improving the anti-tumor activity of T cells. Cancer immunotherapies including the adoptive transfer of naturally occurring tumor-infiltrating lymphocytes (TILs) and genetically engineered T cells, as well as the use of immune checkpoint blockade (ICB) to boost the function of T cells, have emerged as promising approaches to achieve durable clinical responses of otherwise treatment-refractory cancers (Lee et al., 2015; Rosenberg and Restifo, 2015; Sharma and Allison, 2015). Although immunotherapies have been successfully used in the clinic, the number of patients benefiting from them is still limited (Fradet et al., 2019; Newick et al., 2017). Tumor microenvironment (TME)-related immunosuppression has emerged as the major reason for low and/or no response to both immunotherapies (Ninomiya et al., 2015; Schoenfeld and Hellmann, 2020). Therefore, efforts to investigate and overcome TME-related limitations in immune therapies are of great urgency. The fact that immune cells and cancer cells share many fundamental metabolic pathways implies an irreconcilable competition for nutrients in TME (Andrejeva and Rathmell, 2017; Chang et al., 2015). During uncontrolled proliferation, cancer cells hijack alternative pathways for more rapid metabolite generation (Vander Heiden et al., 2009). As a consequence, nutrient depletion, hypoxia, acidity, and generation of metabolites that can be toxic in the TME may hinder successful immunotherapy (Weinberg et al., 2010). Indeed, TILs often experience mitochondrial stress within growing tumors and become exhausted (Scharping et al., 2016). Interestingly, multiple studies also indicate that metabolic changes in TME could re-shape T cell differentiation and functional activity (Bailis et al., 2019; Chang et al., 2013; Peng et al., 2016). All these evidences inspired us to hypothesize that metabolic reprogramming in T cells might rescue them from a stressed metabolic environment, thereby reinvigorating their anti-tumor activity (Buck et al., 2016; Zhang et al., 2017). In this current study, by integrating both genetic and chemical screens, we identified that NAMPT, a key gene involved in NAD+ biosynthesis, was essential for T cell activation. NAMPT inhibition led to robust NAD+ decline in T cells, thereby disrupting glycolysis regulation and mitochondrial function, blocking ATP synthesis, and dampening the T cell receptor (TCR) downstream signaling cascade. Building on the observation that TILs have relatively lower NAD+ and NAMPT expression levels than T cells from peripheral blood mononuclear cells (PBMCs) in ovarian cancer patients, we performed genetic screening in T cells and identified that Tubby (TUB) is a transcription factor for NAMPT. Finally, we applied this basic knowledge in the (pre) clinic and showed very strong evidence that supplementation with NAD+ dramatically improves the anti-tumor killing activity both in adoptively transferred CAR-T cells therapy and immune check point blockade therapy, indicating their promising potential for targeting NAD+ metabolism to better treat cancers. 1.NAD+ regulates the activation of T cells by affecting energy metabolism After antigen stimulation, T cells undergo metabolic reprogramming, from mitochondrial oxidation to glycolysis as the main source of ATP. While maintaining sufficient mitochondrial functions to support cell proliferation and effector functions.Given that NAD+ is the main coenzyme for redox, the researchers verified the effect of NAD+ on the level of metabolism in T cells through experiments such as metabolic mass spectrometry and isotope labeling. The results of in vitro experiments show that NAD+ deficiency will significantly reduce the level of glycolysis, TCA cycle and electron transport chain metabolism in T cells. Through the experiment of replenishing ATP, the researchers found that the lack of NAD+ mainly inhibits the production of ATP in T cells, thereby reducing the level of T cell activation. 2.The NAD+ salvage synthesis pathway regulated by NAMPT is essential for T cell activation The metabolic reprogramming process regulates the activation and differentiation of immune cells. Targeting T cell metabolism provides an opportunity to modulate the immune response in a cellular way. Immune cells in the tumor microenvironment, their own metabolic level will also be correspondingly affected. The researchers in this article have discovered the important role of NAMPT in the activation of T cells through genome-wide sgRNA screening and metabolism-related small molecule inhibitor screening experiments. Nicotinamide adenine dinucleotide (NAD+) is a coenzyme for redox reactions and can be synthesized through the salvage pathway, de novo synthesis pathway, and Preiss-Handler pathway. The NAMPT metabolic enzyme is mainly involved in the NAD+ salvage synthesis pathway. Analysis of clinical tumor samples found that in tumor-infiltrating T cells, their NAD+ levels and NAMPT levels were lower than other T cells. Researchers speculate that NAD+ levels may be one of the factors that affect the anti-tumor activity of tumor-infiltrating T cells. 3.Supplement NAD+ to enhance the anti-tumor activity of T cells Immunotherapy has been exploratory research in cancer treatment, but the main problem is the best treatment strategy and the effectiveness of immunotherapy in the overall population. Researchers want to study whether enhancing the activation ability of T cells by supplementing NAD+ levels can enhance the effect of T cell-based immunotherapy. At the same time, in the anti-CD19 CAR-T therapy model and anti-PD-1 immune checkpoint inhibitor therapy model, it was verified that supplementation of NAD+ significantly enhanced the tumor-killing effect of T cells. The researchers found that in the anti-CD19 CAR-T treatment model, almost all mice in the CAR-T treatment group supplemented with NAD+ achieved tumor clearance, while the CAR-T treatment group without NAD+ supplemented only about 20 % Of mice achieved tumor clearance. Consistent with this, in the anti-PD-1 immune checkpoint inhibitor treatment model, B16F10 tumors are relatively tolerant to anti-PD-1 treatment, and the inhibitory effect is not significant. However, the growth of B16F10 tumors in the anti-PD-1 and NAD+ treatment group could be significantly inhibited. Based on this, NAD+ supplementation can enhance the anti-tumor effect of T cell-based immunotherapy. 4.How to supplement NAD+ The NAD+ molecule is large and cannot be directly absorbed and utilized by the human body. The NAD+ directly ingested orally is mainly hydrolyzed by brush border cells in the small intestine. In terms of thinking, there is indeed another way to supplement NAD+, which is to find a way to supplement a certain substance so that it can synthesize NAD+ autonomously in the human body. There are three ways to synthesize NAD+ in the human body: Preiss-Handler pathway, de novo synthesis pathway and salvage synthesis pathway. Although the three ways can synthesize NAD+, there is also a primary and secondary distinction. Among them, the NAD+ produced by the first two synthetic pathways only accounts for about 15% of the total human NAD+, and the remaining 85% is achieved through the way of remedial synthesis. In other words, the salvage synthesis pathway is the key to the human body to supplement NAD+. Among the precursors of NAD+, nicotinamide (NAM), NMN and nicotinamide ribose (NR) all synthesize NAD+ through a salvage synthesis pathway, so these three substances have become the body's choice for supplementing NAD+. Although NR itself has no side effects, in the process of NAD+ synthesis, most of it is not directly converted into NMN, but needs to be digested into NAM first, and then participate in the synthesis of NMN, which still cannot escape the limitation of rate-limiting enzymes. Therefore, the ability to supplement NAD+ through oral administration of NR is also limited . As a precursor for supplementing NAD+, NMN not only bypasses the restriction of rate-limiting enzymes, but is also absorbed very quickly in the body and can be directly converted into NAD+. Therefore, it can be used as a direct, rapid and effective method to supplement NAD+. Expert Reviews: Xu Chenqi (Excellence and Innovation Center of Molecular Cell Science, Chinese Academy of Sciences, Immunology Research Expert) Cancer treatment is a problem in the world. The development of immunotherapy has made up for the limitations of traditional cancer treatment and expanded the treatment methods of doctors. Cancer immunotherapy can be divided into immune checkpoint blocking therapy, engineered T cell therapy, tumor vaccine, etc. These treatment methods have played a certain role in the clinical treatment of cancer. At the same time, this also makes the current focus of immunotherapy research on how to further enhance the effect of immunotherapy and expand the beneficiaries of immunotherapy.
Razkrivanje vplivov zdravljenja z ginsenozidom Rg3 na poškodbe NPC-jev, ki jih povzroča IL-1β
Uvod Degeneracija medvretenčne ploščice (IDD) je pogosto opažena ortopedska bolezen, ki jo spremlja prekomerna apoptoza celic jedra pulposusa (NPC) in degeneracija zunajceličnega matriksa (ECM), z glavnimi simptomi bolečine in odrevenelosti v pasu, nogah in stopalih ter vnetja na in okoli površine kostnega tkiva. Presenetljivo je, da je bilo potrjeno, da ginsenozid Rg3, glavna aktivna sestavina ginsenga, kaže antikatabolične in antiapoptotične učinke pri človeških NPC-jih, zdravljenih z IL-1β, in podganah IDD, z inaktiviranjem poti p38 MAPK. Dejavniki tveganja za IDD IDD je na splošno povezan z dejavniki tveganja, kot so staranje, prekomerna vadba, delovno okolje in genetika. Ko se človek stara, se bo količina vode v telesu in v medvretenčnih diskih ustrezno zmanjšala. Medvretenčni diski, ki nimajo vlage, bodo izgubili svojo elastično funkcijo in postali trdi. Ko pride do stimulacije ali pritiska, se lahko medvretenčni disk razpoči, kar povzroči poškodbo medvretenčnega diska. Na primer, mehanska travma, ki jo povzroča prekomerna vadba in delo, lahko pospeši krhkost diska in poslabša IDD. Antikatabolični in antiapoptotični učinki ginsenozida Rg3 pri človeških NPC, zdravljenih z IL-1β, in podganah IDD Ginsenozid Rg3 ima antiapoptotično vlogo pri človeških NPC-jih, zdravljenih z IL-1β, in podganah IDD, kar dokazuje znižanje pro-apoptoznega proteina Bax in navzgor regulacija antiapoptoznega proteina Bcl-2 pri IL-1β-stimuliranih NPC-jih in podganah IDD. Poleg tega ginsenozid Rg3 zavira razgradnjo ECM v IL-1β stimuliranih NPC-jih in tkivih medvretenčnih diskov podgan IDD, kar potrjuje zmanjšana ekspresija faktorjev, povezanih z razgradnjo ECM, MMP (MMP2 in MMP3) in ADAMTS (Adamts4 in Adamts5). Ginsenozid Rg3 kaže antikatabolične in antiapoptotične učinke pri človeških NPC, zdravljenih z IL-1β. Ginsenozid Rg3 zmanjšuje apoptozo in katabolizem pri podganah z IDD. Lajšanje ginsenozida Rg3 v IDD po poti p38 MAPK Ginsenozid Rg3 lahko ublaži degeneracijo NPC, obnovi razporeditev vlaknastega obroča in ohrani več proteoglikanskega matriksa z inaktiviranjem poti p38 MAPK. In vitro je intenzivnost fluorescence p38 povečana pri NPC-jih, ki jih stimulira IL-1β, vendar ginsenozid Rg3 izravna ta promocijski učinek. In vivo je fosforilirana raven p38 povišana v NPC in tkivih medvretenčnih diskov podgan IDD, medtem ko ginsenozid Rg3 deluje obratno. Ginsenozid Rg3 zavira IL-1β-stimulirano pot p38 MAPK pri človeških NPC Ginsenozid Rg3 inaktivira pot p38 MAPK pri podganah IDD. Sklep Antikatabolični in antiapoptotični učinki ginsenozida Rg3 v celicah človeškega jedra pulposusa, zdravljenih z IL-1β, in v podganjem modelu degeneracije diska, se dosežejo z inaktiviranjem poti MAPK, kar zagotavlja nove namige o zdravljenju IDD. Referenčni Ginsenoside Rg3 kaže antikatabolične in antiapoptotične učinke v celicah človeškega jedra pulposusa, obdelanih z IL-1β, in v podganjem modelu degeneracije diska z inaktiviranjem poti MAPK. Cell Mol Biol. 2024; 70(1):233-238. doi:10.14715/cmb/2024.70.1.32 BONTAC Ginsenosides BONTAC se od leta 2012 posveča raziskavam in razvoju, proizvodnji in prodaji surovin za koencime in naravne izdelke, z lastnimi tovarnami, več kot 170 globalnimi patenti in močno ekipo za raziskave in razvoj. BONTAC ima bogate izkušnje na področju raziskav in razvoja ter napredno tehnologijo na področju biosinteze redkih ginsenozidov Rh2/Rg3 s čistimi surovinami, višjo stopnjo pretvorbe in višjo vsebnostjo (do 99%). Storitev na enem mestu za prilagojeno rešitev izdelka je na voljo v podjetju BONTAC. Z edinstveno tehnologijo encimske sinteze Bonzyme lahko tukaj natančno sintetiziramo izomere tipa S in R, z močnejšo aktivnostjo in natančnim ciljnim delovanjem. Naši izdelki so podvrženi strogemu samopregledu tretjih oseb, ki je vreden zaupanja vrednega. Disclaimer Ta članek temelji na referenci v akademski reviji. Ustrezne informacije so na voljo samo za namene izmenjave in učenja in ne predstavljajo nobenih medicinskih nasvetov. Če pride do kršitve, se za izbris obrnite na avtorja. Stališča, izražena v tem članku, ne predstavljajo stališča skupine BONTAC. BONTAC v nobenem primeru ne bo odgovoren za kakršne koli zahtevke, škodo, izgube, izdatke ali stroške, ki izhajajo ali izhajajo neposredno ali posredno iz vašega zanašanja na informacije in gradivo na tej spletni strani.
NR as a Promising Therapeutic Candidate for Alpers' Disease
Introduction Alpers' disease is both a neurodegenerative disorder and a metabolic disorder, which is tightly linked to mitochondrial dysfunction and mutations in the catalytic subunit of polymerase gamma (POLG) gene. Noteworthily, supplementation of NAD precursor, nicotinamide riboside (NR), is evidenced to explicitly ameliorate mitochondrial defects in cortical organoids of patients with Alpers' disease. About Alpers’ disease Alpers’ disease is an autosomal recessive disorder, which is often accompanied with cortical neuronal loss as well as depletion of mitochondrial DNA (mtDNA) and complex I (CI). The disease occurs in about 1 in 100,000 newborns. Most individuals with Alpers’ disease show no symptoms at birth. Diagnosis is generally established by determining the POLG gene. Once onset (usually between first and third years of life), patients may present the symptoms such as progressive encephalopathy, epilepsy, myoclonus, and myasthenia gravis. Currently, there is no effective method to cure this disease. Establishment of Alpers' disease model in vitro Induced pluripotent stem cells (iPSCs) are generated from Alpers' patient carrying the compound heterozygous mutations of A467T (c.1399G>A) and P589L (c.1766C>T), followed by differentiation into cortical organoids and neural stem cells (NSCs). Alpers's iPSCs exhibit mild mitochondrial alterations, including an elevated L-lactate level and a depletion of CI. Alpers' NSCs manifest profound mtDNA depletion and mitochondrial dysfunction. Alpers' cortical organoids demonstrate cortical neuronal loss and astrocyte accumulation. The role of NR in Alpers' cortical organoids Long-term treatment with NR partially ameliorates the neurodegenerative alterations observed in Alpers' cortical organoids. Specifically, supplementation of NR effectively counteracts neuronal loss, glial enrichment, and mitochondrial damage observed in cortical organoids of patients with Alpers' disease. Reversal of the dysregulated pathways in Alpers' patient organoids post NR treatment NR treatment offsets the downregulation of mitochondrial and synaptogenesis-related pathways, as well as upregulation of pathways associated with astrocyte/glial cells and neuroinflammation are obviously activated in Alpers' cortical organoids. Conclusion Replenishment of NR to increase NAD level can rescue mitochondrial defects and neuronal loss in iPSC-derived cortical organoid of Alpers’ disease, with relatively high safety and bioavailability, showing great promise as a therapeutic candidate for this intractable disorder. Reference Hong Y, Zhang Z, Yangzom T, et al. The NAD+ Precursor Nicotinamide Riboside Rescues Mitochondrial Defects and Neuronal Loss in iPSC derived Cortical Organoid of Alpers' Disease. Int J Biol Sci. 2024;20(4):1194-1217. Published 2024 Jan 25. doi:10.7150/ijbs.91624 BONTAC NR BONTAC is one of the few suppliers in China that can launch mass production of raw materials for NR, with self-owned factory and professional R&D team. Up till now, there are 173 BONTAC patents. BONTAC provides one-stop service for customized products. Both malate and chloride salt forms of NR are available. By dirt of unique Bonpure seven-step purification technology and Bonzyme Whole-enzymatic method, the product content and conversion rate can be maintained in a higher level. The purity of BONTAC NR can reach above 97%. Our products are subjected to strict third-party self-inspection, which are worth of trustworthy. Disclaimer This article is based on the reference in the academic journal. The relevant information is provided for sharing and learning purposes only, and does not represent any medical advice purposes. If there is any infringement, please contact the author for deletion. The opinions expressed in this article do not represent the position of BONTAC. Under no circumstances will BONTAC be held responsible or liable in any way for any claims, damages, losses, expenses, costs or liabilities whatsoever (including, without limitation, any direct or indirect damages for loss of profits, business interruption or loss of information) resulting or arising directly or indirectly from your reliance on the information and material on this website.