Acetylcholine chloride
Acetylcholine Chloride is a neurotransmitter in both the peripheral nervous system (PNS) and central nervous system (CNS) in many organisms including humans. Acetylcholine chloride in micromolar concentrations significantly inhibit p53 mutant peptide aggregation in vitro, and could be promising candidate for p53 mutant/ misfolded protein aggregation inhibition, and mutations of tumor suppressor protein p53 are present in almost about 50% of all cancers.
Inquire / Order:
manager@chemfaces.com
Technical Inquiries:
service@chemfaces.com
Tel:
+86-27-84237783
Fax:
+86-27-84254680
Address:
1 Building, No. 83, CheCheng Rd., Wuhan Economic and Technological Development Zone, Wuhan, Hubei 430056, PRC
Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com
The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
Food Chem.2020, 327:126992.
LWT2020, 124:109163
Dermatologica Sinica2024, 42(1):p19-30.
Biomed Pharmacother.2023, 166:115329.
BMC Cancer. 2021, 21(1):91.
Cell Death Dis.2019, 10(12):882
J Cell Biochem.2024, 125(4):e30537.
J Pharm Pharmacol.2022, rgac033.
Biosci. Rep.2020, 10.1024
Pharmaceuticals (Basel).2020, 13(9):262.
Related and Featured Products
Protein Pept Lett. 2017;24(4):353-357.
Inhibition of p53 Mutant Peptide Aggregation In Vitro by Cationic Osmolyte Acetylcholine Chloride.[Pubmed:
28117010]
Mutations of tumor suppressor protein p53 are present in almost about 50% of all cancers. It has been reported that the p53 mutations cause aggregation and subsequent loss of p53 function, leading to cancer progression.
METHODS AND RESULTS:
Here in this study we focus on the inhibitory effects of cationic osmolyte molecules Acetylcholine chloride, and choline on an aggregation prone 10 amino acid p53 mutant peptide WRPILTIITL, and the corresponding wildtype peptide RRPILTIITL in vitro. The characterization tools used for this study include Thioflavin- T (ThT) induced fluorescence, transmission electron microscopy (TEM), congo red binding, turbidity, dynamic light scattering (DLS), and cell viability assays.
CONCLUSIONS:
The results show that Acetylcholine chloride in micromolar concentrations significantly inhibit p53 mutant peptide aggregation in vitro, and could be promising candidate for p53 mutant/ misfolded protein aggregation inhibition.
Microvasc Res. 2011 Sep;82(2):190-7.
Acetylcholine chloride as a potential source of variability in the study of cutaneous vascular function in man.[Pubmed:
21601579]
Laser-Doppler flowmetry (LDF) coupled with Acetylcholine chloride (ACh) iontophoresis is increasingly recognized as a reliable non-invasive method to study the endothelial function. However, Acetylcholine chloride-vasodilation measurement appears highly variable possibly due to the Acetylcholine chloride pharmacological properties itself. These problems may be partially overcome by using methacholine chloride (MCh), a more stable synthetic agonist of muscarinic receptors, instead of Acetylcholine chloride. Therefore, we first studied the correlation between the two drugs and then the effects of (1) spatial variability (inter-site measurements), (2) temporal variability (inter-day measurements), (3) intra-day variability (morning versus evening), and (4) age on the variability of both Acetylcholine chloride-vasodilation and MCh-vasodilation.
METHODS AND RESULTS:
The endothelium-dependent vasodilation response to simultaneous iontophoretic applications (4 doses of 10s at 0.1mA with 2min of current-free interval) of Acetylcholine chloride(11mM) or MCh (10mM) was studied on the forearm of 40 healthy subjects (36 males, median 28yr, range 21-59yr). The percent change in perfusion (CVCpeak) from baseline and the area under the curve (CVC(AUC)) during iontophoresis were assessed. Inter-site, inter-day and intra-day coefficients of variation (CV) were studied for each drug as well as correlations between drugs and age. A linear relationship was found between ACh- and MCh-CVCpeak (r²=0.75, p=0.01) and between ACh- and MCh-CVC(AUC) (r²=0.55, p=0.02). MCh inter-site CV for both CVCpeak (12.2%) and CVC(AUC) (13.8%) was significantly lower than ACh inter-site CV for CVCpeak (15.5%) and CVC(AUC) (15.3%), respectively. MCh inter-day CV for CVCpeak (17.2%) and CVC(AUC) (14.6%) was significantly lower than ACh inter-day CV for CVCpeak (19.7%) and ACh CVC(AUC) (21.2%). For ACh and MCh, the CVCpeak and CVC(AUC) were higher at 16:00pm than at 11:00am (p<0.05 for all). Finally, both ACh- and MCh-CVCpeak exhibited a logarithmic decrease with age (r²=0.61, p<0.01 and r²=0.58, p<0.01).
CONCLUSIONS:
Although both drugs exhibited circadian and age variability, MCh exhibited less inter-site and interday variabilities than did Acetylcholine chloride for the evaluation of cutaneous endothelium-dependent vasodilation. These findings should be taken into account in studies of cutaneous vascular function by iontophoresis coupled with laser Doppler flowmetry.
