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ACDPP hydrochloride

Selective mGlu5 receptor antagonist CAS# 37804-11-8

ACDPP hydrochloride

Catalog No. BCC7302----Order now to get a substantial discount!

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Chemical structure

ACDPP hydrochloride

3D structure

Chemical Properties of ACDPP hydrochloride

Cas No. 37804-11-8 SDF Download SDF
PubChem ID 16759168 Appearance Powder
Formula C12H14Cl2N6O M.Wt 329.19
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 100 mM in DMSO
Chemical Name 3-amino-6-chloro-5-(dimethylamino)-N-pyridin-3-ylpyrazine-2-carboxamide;hydrochloride
SMILES CN(C)C1=NC(=C(N=C1Cl)C(=O)NC2=CN=CC=C2)N.Cl
Standard InChIKey CXIHLPLRTFPHKX-UHFFFAOYSA-N
Standard InChI InChI=1S/C12H13ClN6O.ClH/c1-19(2)11-9(13)17-8(10(14)18-11)12(20)16-7-4-3-5-15-6-7;/h3-6H,1-2H3,(H2,14,18)(H,16,20);1H
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of ACDPP hydrochloride

DescriptionAntagonist at the mGlu5 receptor (Ki = 295 nM). Inhibits human mGlu5 receptor-mediated calcium flux with an IC50 of 134 nM.

ACDPP hydrochloride Dilution Calculator

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ACDPP hydrochloride Molarity Calculator

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Preparing Stock Solutions of ACDPP hydrochloride

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.0378 mL 15.1888 mL 30.3776 mL 60.7552 mL 75.944 mL
5 mM 0.6076 mL 3.0378 mL 6.0755 mL 12.151 mL 15.1888 mL
10 mM 0.3038 mL 1.5189 mL 3.0378 mL 6.0755 mL 7.5944 mL
50 mM 0.0608 mL 0.3038 mL 0.6076 mL 1.2151 mL 1.5189 mL
100 mM 0.0304 mL 0.1519 mL 0.3038 mL 0.6076 mL 0.7594 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on ACDPP hydrochloride

Unusual 4-arsonoanilinium cationic species in the hydrochloride salt of (4-aminophenyl)arsonic acid and formed in the reaction of the acid with copper(II) sulfate, copper(II) chloride and cadmium chloride.[Pubmed:28378716]

Acta Crystallogr C Struct Chem. 2017 Apr 1;73(Pt 4):325-330.

Structures having the unusual protonated 4-arsonoanilinium species, namely in the hydrochloride salt, C6H9AsNO3(+).Cl(-), (I), and the complex salts formed from the reaction of (4-aminophenyl)arsonic acid (p-arsanilic acid) with copper(II) sulfate, i.e. hexaaquacopper(II) bis(4-arsonoanilinium) disulfate dihydrate, (C6H9AsNO3)2[Cu(H2O)6](SO4)2.2H2O, (II), with copper(II) chloride, i.e. poly[bis(4-arsonoanilinium) [tetra-mu-chlorido-cuprate(II)]], {(C6H9AsNO3)2[CuCl4]}n, (III), and with cadmium chloride, i.e. poly[bis(4-arsonoanilinium) [tetra-mu-chlorido-cadmate(II)]], {(C6H9AsNO3)2[CdCl4]}n, (IV), have been determined. In (II), the two 4-arsonoanilinium cations are accompanied by [Cu(H2O)6](2+) cations with sulfate anions. In the isotypic complex salts (III) and (IV), they act as counter-cations to the {[CuCl4](2-)}n or {[CdCl4](2-)}n anionic polymer sheets, respectively. In (II), the [Cu(H2O)6](2+) ion sits on a crystallographic centre of symmetry and displays a slightly distorted octahedral coordination geometry. The asymmetric unit for (II) contains, in addition to half the [Cu(H2O)6](2+) ion, one 4-arsonoanilinium cation, a sulfate dianion and a solvent water molecule. Extensive O-H...O and N-H...O hydrogen bonds link all the species, giving an overall three-dimensional structure. In (III), four of the chloride ligands are related by inversion [Cu-Cl = 2.2826 (8) and 2.2990 (9) A], with the other two sites of the tetragonally distorted octahedral CuCl6 unit occupied by symmetry-generated Cl-atom donors [Cu-Cl = 2.9833 (9) A], forming a two-dimensional coordination polymer network substructure lying parallel to (001). In the crystal, the polymer layers are linked across [001] by a number of bridging hydrogen bonds involving N-H...Cl interactions from head-to-head-linked As-O-H...O 4-arsonoanilinium cations. A three-dimensional network structure is formed. Cd(II) compound (IV) is isotypic with Cu(II) complex (III), but with the central CdCl6 complex repeat unit having a more regular M-Cl bond-length range [2.5232 (12)-2.6931 (10) A] compared to that in (III). This series of compounds represents the first reported crystal structures having the protonated 4-arsonoanilinium species.

Lens opacities in children using methylphenidate hydrochloride.[Pubmed:28376677]

Cutan Ocul Toxicol. 2017 Dec;36(4):362-365.

PURPOSE: To assess clinical findings of eye examination in children having attention deficit hyperactivity disorder (ADHD) administered with methylphenidate hydrochloride. METHODS: Fifty-seven consecutive patients diagnosed of ADHD and administered with oral methylphenidate hydrochloride treatment for at least one year were involved in this study (Group 1). Sixty healthy subjects (Group 2) having demographic features similar to group 1 were involved as a control group. All patients underwent detailed ophthalmological examination. RESULTS: One hundred and seventeen consecutive subjects with a mean age of 11.2 +/- 2.4 years (7-18 years) were enrolled. Fifty-seven consecutive patient (32 males, 25 females) under oral methylphenidate hydrochloride treatment (Group 1) and 60 healthy control subjects (30 males, 30 females) (Group 2)) were recruited for this prospective study. The mean methylphenidate hydrochloride dosage was 0.9 +/- 0.1 mg/kg/day and the mean duration of methylphenidate hydrochloride usage was for 2.73 +/- 0.73 years (1-7 years). High intraocular pressure was not observed in any of the patients in our study. We detected lens opacities in five eyes of five patients in group 1 (p = 0.019). The patient with the highest degree of cataract formation had been using MPH for 84 months and this patient's cataract score was P4. CONCLUSION: Long-term use of methylphenidate may cause lens opacities. In particular, patients who have been using methylphenidate for more than two years should go for regular eye examination.

Biophysical Study on the Interaction between Eperisone Hydrochloride and Human Serum Albumin Using Spectroscopic, Calorimetric, and Molecular Docking Analyses.[Pubmed:28380300]

Mol Pharm. 2017 May 1;14(5):1656-1665.

Eperisone hydrochloride (EH) is widely used as a muscle relaxant for patients with muscular contracture, low back pain, or spasticity. Human serum albumin (HSA) is a highly soluble negatively charged, endogenous and abundant plasma protein ascribed with the ligand binding and transport properties. The current study was undertaken to explore the interaction between EH and the serum transport protein, HSA. Study of the interaction between HSA and EH was carried by UV-vis, fluorescence quenching, circular dichroism (CD), Fourier transform infrared (FTIR) spectroscopy, Forster's resonance energy transfer, isothermal titration calorimetry and differential scanning calorimetry. Tryptophan fluorescence intensity of HSA was strongly quenched by EH. The binding constants (Kb) were obtained by fluorescence quenching, and results show that the HSA-EH interaction revealed a static mode of quenching with binding constant Kb approximately 10(4) reflecting high affinity of EH for HSA. The negative DeltaG degrees value for binding indicated that HSA-EH interaction was a spontaneous process. Thermodynamic analysis shows HSA-EH complex formation occurs primarily due to hydrophobic interactions, and hydrogen bonds were facilitated at the binding of EH. EH binding induces alpha-helix of HSA as obtained by far-UV CD and FTIR spectroscopy. In addition, the distance between EH (acceptor) and Trp residue of HSA (donor) was calculated 2.18 nm using Forster's resonance energy transfer theory. Furthermore, molecular docking results revealed EH binds with HSA, and binding site was positioned in Sudlow Site I of HSA (subdomain IIA). This work provides a useful experimental strategy for studying the interaction of myorelaxant with HSA, helping to understand the activity and mechanism of drug binding.

Fabrication yields of serially harvested calf-fed Holstein steers fed zilpaterol hydrochloride.[Pubmed:28380524]

J Anim Sci. 2017 Mar;95(3):1209-1218.

Holstein steers ( = 110) were fed zilpaterol hydrochloride (ZH) for 0 or 20 d before slaughter during a 280-d serial harvest study. Cattle were harvested every 28 d beginning at 254 d on feed (DOF) and concluding at 534 DOF. After slaughter, carcasses were chilled for 48 h and then fabricated into boneless closely trimmed or denuded subprimals, lean trim, trimmable fat, and bone. Inclusion of ZH increased cold side weight (CSW) by 10.3 kg ( < 0.01; 212.7 vs. 202.4 kg [SEM 1.96]) and saleable yield by 10.4 kg ( < 0.01; 131.9 vs. 121.5 kg [SEM 1.16]) in calf-fed Holstein steer carcasses. Additionally, saleable yield as a percentage of CSW increased (

Roles of calcium-stimulated adenylyl cyclase and calmodulin-dependent protein kinase IV in the regulation of FMRP by group I metabotropic glutamate receptors.[Pubmed:18434517]

J Neurosci. 2008 Apr 23;28(17):4385-97.

The fragile X syndrome is caused by the lack of fragile X mental retardation protein (FMRP) attributable to silencing of the FMR1 gene. The metabotropic glutamate receptors (mGluRs) in the CNS contribute to different brain functions, including learning/memory, mental disorders, drug addiction, and persistent pain. Most of the previous studies have been focused on downstream targets of FMRP in hippocampal neurons, and fewer studies have been reported for the second-messenger signaling pathways between group I mGluRs and FMRP. Furthermore, no molecular study has been performed in the anterior cingulate cortex (ACC), a key region involved in high brain cognitive and executive functions. In this study, we demonstrate that activation of group I mGluR upregulated FMRP in ACC neurons of adult mice through the Ca(2+)-dependent signaling pathways. Using genetic approaches, we found that Ca(2+)/calmodulin-stimulated adenylyl cyclase 1 (AC1) and calcium/calmodulin-dependent kinase IV (CaMKIV) contribute to the upregulation of FMRP induced by stimulating group I mGluRs. The upregulation of FMRP occurs at the transcriptional level. The cAMP-dependent protein kinase is activated by stimulating group I mGluRs through AC1 in ACC neurons. Both AC1 and CaMKIV contribute to the regulation of FMRP by group I mGluRs probably through cAMP response element-binding protein activation. Our study has provided the first evidence for a molecular link between group I mGluRs and FMRP in ACC neurons and may help us to understand the pathogenesis of fragile X syndrome.

Dipyridyl amides: potent metabotropic glutamate subtype 5 (mGlu5) receptor antagonists.[Pubmed:15686941]

Bioorg Med Chem Lett. 2005 Feb 15;15(4):1197-200.

The mGlu5 receptor has been implicated in a number of CNS disorders. Herein, we report on the discovery, synthesis, and biological evaluation of dipyridyl amides as small molecules mGluR5 antagonists.

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