Ascorbic Acid (30-300mesh Crystal Powder)
Ascorbic Acid (30-300mesh Crystal Powder)
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Ascorbic Acid (30-300mesh Crystal Powder)

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Catalog Number PR50817-1
CAS 50-81-7
Synonyms L-Ascorbic acid; L-Threoascorbic acid
IUPAC Name (2R)-2-[(1S)-1,2-dihydroxyethyl]-3,4-dihydroxy-2H-furan-5-one
Molecular Weight 176.12
Molecular Formula C6H8O6
InChI InChI=1S/C6H8O6/c7-1-2(8)5-3(9)4(10)6(11)12-5/h2,5,7-10H,1H2/t2-,5+/m0/s1
InChI Key CIWBSHSKHKDKBQ-JLAZNSOCSA-N
EC Number 200-066-2
Isomeric SMILES C([C@@H]([C@@H]1C(=C(C(=O)O1)O)O)O)O
MDL Number MFCD00064328
Packaging 25kg/carton
Standard USP/BP/EP/JP/JSFA/FCC/E300
Case Study

High-Dose Ascorbic Acid as an Adjunctive Therapy for Patients with Septic Shock

Zabet, Mohadeseh Hosseini, et al. Journal of research in pharmacy practice, 2016, 5(2), 94-100.

This paper evaluated whether high-dose ascorbic acid reduced vasopressor needs in severely ill surgical patients in septic shock. The findings indicated that high dose ascorbic acid is a feasible and safe adjunctive therapy for terminally ill surgical patients in septic shock.
· Evaluation methods
Septic shock patients requiring vasopressor therapy for keeping mean arterial pressure above 65 mmHg were randomly assigned to 25 mg/kg intravenous ascorbic acid every six hours or the equivalent placebo for 72 hours. Those were the main measures: vasopressor dose and duration; secondary measures: duration in ICU and 28-day mortality.
· Results
There were 28 patients in the trial (14 in each group). The mean norepinephrine dose during the study was much lower in the ascorbic acid group than in the placebo group (7.44 3.65 mcg/min vs 13.79 6.48 mcg/min, P = 0.004). So too was the duration of norepinephrine treatment in the ascorbic acid group (49.64 25.67 vs 71.57 1.60 hours, P = 0.007). Although ICU duration didn't differ significantly between the two groups, the 28-day mortality was lower in the ascorbic acid group than in the placebo group (14.28% vs. 64.28%; P = 0.009).

Effect of Ascorbic Acid on Osteogenic Differentiation of Stem Cells in Vitro

Langenbach, Fabian, et al. Stem cell research & therapy, 2013, 4, 1-7.

The usual osteogenic differentiation protocol for pluripotent stem cells is to treat confluent monolayers with a solution of dexamethasone (Dex), ascorbic acid (Asc) and -glycerophosphate (-Gly). This article detailed how these chemicals affect the intracellular signaling pathways that result in osteogenic differentiation of bone marrow stromal stem cells. Among them, Asc causes the production of more type I collagen (Col1), which leads to more intracellular signalling via Col1/α2β1 integrin.
Function of ascorbic acid in osteogenic differentiation
What makes Asc so essential to osteogenic differentiation is the release of collagen type I (Col1) into the ECM. For example, osteogenic differentiation of human bone marrow stromal cells (BMSCs) occurred most successfully at 50 M ascorbic acid-2-phosphate, a more stable form of Asc in conventional culture conditions.
A model was developed to explain how the ECM initiates and maintains osteoblast differentiation: (1) Osteoblasts need contact with a collagen-containing ECM to start to differentiate. (2) They stick to this ECM through Col1 and α2β1 integrin interaction. (3) Integrin ligands activate MAPK signaling networks, which transmit messages to the nucleus. (4) MAPK phosphorylates and activates Runx2 which then acts to induce osteoblast differentiation by stimulating transcription of osteoblast marker genes like osteocalcin.

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