1. Immunology/Inflammation
    NF-κB
    Metabolic Enzyme/Protease
    Neuronal Signaling
    Membrane Transporter/Ion Channel
    Apoptosis
  2. Reactive Oxygen Species
    Calcium Channel
    Apoptosis
    Endogenous Metabolite
  3. L-Ascorbic acid

L-Ascorbic acid (Synonyms: L-Ascorbate; Vitamin C)

Cat. No.: HY-B0166 Purity: 99.92%
Handling Instructions

L-Ascorbic acid (L-Ascorbate), an electron donor, is an endogenous antioxidant agent. L-Ascorbic acid inhibits selectively Cav3.2 channels with an IC50 of 6.5 μM. L-Ascorbic acid is also a collagen deposition enhancer and an elastogenesis inhibitor. L-Ascorbic acid exhibits anti-cancer effects through the generation of reactive oxygen species (ROS) and selective damage to cancer cells.

For research use only. We do not sell to patients.

L-Ascorbic acid Chemical Structure

L-Ascorbic acid Chemical Structure

CAS No. : 50-81-7

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Based on 18 publication(s) in Google Scholar

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Description

L-Ascorbic acid (L-Ascorbate), an electron donor, is an endogenous antioxidant agent. L-Ascorbic acid inhibits selectively Cav3.2 channels with an IC50 of 6.5 μM. L-Ascorbic acid is also a collagen deposition enhancer and an elastogenesis inhibitor[1][2][3]. L-Ascorbic acid exhibits anti-cancer effects through the generation of reactive oxygen species (ROS) and selective damage to cancer cells[4].

IC50 & Target

Microbial Metabolite

 

In Vitro

The anti-cancer effects of L-Ascorbic acid are determined by sodium-dependent vitamin C transporter 2 (SVCT-2), a transporter of L-ascorbic acid. L-Ascorbic acid (0.1 μM-2 mM) exhibits anti-cancer effects according to SVCT-2 expression and L-ascorbic acid uptake. Human colorectal cancer cell lines displays differential responses to L-ascorbic acid, primarily depending on the expression level of SVCT-2[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[4]

Cell Line: High SVCT-2 expressing cell lines Sw620, Sw480, LoVo, SNU-C4; Low SVCT-2 expressing cell lines HCT15, HCT116, DLD-1, CoLo-205
Concentration: 0, 0.1 μM, 1 μM, 10 μM, 0.1 mM, 0.5 mM, 1 mM, and 2 mM
Incubation Time: 24 hours
Result: Some high SVCT-2 expressing cancer cells demonstrated a dramatic cell-autonomous inhibitory effect of L-ascorbic acid.
Low SVCT-2 expressing cell lines showed biphasic responses to L-ascorbic acid.

Western Blot Analysis[4]

Cell Line: Sw620, Sw480, LoVo, SNU-C4, HCT15, HCT116, DLD-1, CoLo-205 cell lines
Concentration: 1 mM
Incubation Time:
Result: The cell lines showed different levels of SVCT-2 expression in western blot analyses: Sw620, Sw480, and Lovo expressed high levels of SVCT-2 whereas HCT116, HCT15, and DLD-1 expressed low levels.
In Vivo

L-Ascorbic acid/Tolbutamide produces hypoglycaemic activity in a dose dependant manner in normal (60 mg/kg) and diabetic (40 mg/kg) condition. In the presence of L-ascorbic acid, Tolbuatmide (20 mg/kg) produces early onset of action and maintained for longer period compared to Tolbutamide matching control[5].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Normal rats:Albino rats of either sex weighing between 125-175 g[5]
Dosage: Group I received L-ascorbic acid 60 mg/kg, Group II received Tolbutamide 20 mg/kg and Group III was given L-ascorbic acid (60 mg/kg) prior to the administration of tolbutamide 20 mg/kg
Administration: Administered orally
Result: L-ascorbic acid at the dose of 60 mg/kg produced 50.91% blood glucose reduction at 0.5 h and 20 mg/kg body weight of Tolbutamide produced 33% at 4 h as peak effects. In the presence of L-ascorbic acid (60 mg/kg), the action of Tolbutamide was early in onset and maintained for 6 h.
Animal Model: Diabetic rats:Albino rats of either sex weighing between 125 to 175 g were fasted overnight before injection with Alloxan[5]
Dosage: Group I received L-ascorbic acid 40 mg/kg and Group II received Tolbutamide 20 mg/kg while Group III was given L-ascorbic acid 40 mg/kg prior to Tolbutamide administration (20 mg/kg).
Administration: Oral administration
Result: L-ascorbic acid (40 mg/kg alone) produced 42.53% blood glucose reduction at 1.5 h and Tolbutamide 20 mg/kg produced 45.09 at 4 h. Administration of L-ascorbic acid 40 mg/kg body weight prior to Tolbutamide produced antidiabetic activity at 0.5 h and was maintained for 6 h.
Clinical Trial
Molecular Weight

176.12

Formula

C₆H₈O₆

CAS No.
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Solvent & Solubility
In Vitro: 

H2O : ≥ 100 mg/mL (567.79 mM)

DMSO : 100 mg/mL (567.79 mM; Need ultrasonic)

*"≥" means soluble, but saturation unknown.

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 5.6779 mL 28.3897 mL 56.7795 mL
5 mM 1.1356 mL 5.6779 mL 11.3559 mL
10 mM 0.5678 mL 2.8390 mL 5.6779 mL
*Please refer to the solubility information to select the appropriate solvent.
References

Purity: 99.92%

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L-Ascorbic acid
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