TMPH hydrochlorideNeuronal nicotinic receptor antagonist CAS# 849461-91-2 |
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Quality Control & MSDS
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Chemical structure
3D structure
Cas No. | 849461-91-2 | SDF | Download SDF |
PubChem ID | 16079014 | Appearance | Powder |
Formula | C16H32ClNO2 | M.Wt | 305.88 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | Soluble to 100 mM in water and to 100 mM in DMSO | ||
Chemical Name | (2,2,6,6-tetramethylpiperidin-4-yl) heptanoate;hydrochloride | ||
SMILES | CCCCCCC(=O)OC1CC(NC(C1)(C)C)(C)C.Cl | ||
Standard InChIKey | XIDDVJIJIFWGIX-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C16H31NO2.ClH/c1-6-7-8-9-10-14(18)19-13-11-15(2,3)17-16(4,5)12-13;/h13,17H,6-12H2,1-5H3;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. |
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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. |
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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. |
Description | Potent non-competitive antagonist of neuronal nicotinic ACh receptors (nAChRs). Produces long-lasting inhibition of neuronal nAChRs formed by the combination of the most abundant α and β subunits (i.e. α3, α4 and β2, β4 respectively). Displays little inhibition of muscle-type (α1β1γδ) or α7 receptors. |
TMPH hydrochloride Dilution Calculator
TMPH hydrochloride Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.2693 mL | 16.3463 mL | 32.6926 mL | 65.3851 mL | 81.7314 mL |
5 mM | 0.6539 mL | 3.2693 mL | 6.5385 mL | 13.077 mL | 16.3463 mL |
10 mM | 0.3269 mL | 1.6346 mL | 3.2693 mL | 6.5385 mL | 8.1731 mL |
50 mM | 0.0654 mL | 0.3269 mL | 0.6539 mL | 1.3077 mL | 1.6346 mL |
100 mM | 0.0327 mL | 0.1635 mL | 0.3269 mL | 0.6539 mL | 0.8173 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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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 ( = 0.01) by 2.19% (62.64 vs. 60.45% [SEM 0.22]) for cattle supplemented with ZH. Subprimal weights were heavier ( = 0.05) from cattle that received ZH except for the bottom sirloin ball tip, back ribs, and outside skirt regardless of slaughter endpoint. Yield of top round, bottom round, and knuckle was increased ( = 0.01) following ZH supplementation by 0.37, 0.24, and 0.18%, respectively. Yield of the top sirloin butt, strip loin, and tenderloin was increased ( = 0.01) concurrent with ZH supplementation by 0.18, 0.11, and 0.09%, respectively. Regarding the rib primal, the rib eye roll tended ( = 0.08) to had increased yield (2.80 vs. 2.72% [SEM 0.03]) with ZH supplementation; both back ribs and blade meat exhibited increased ( = 0.04) yields of 0.04%. Relative to the chuck primal, increased ( = 0.03) yields of shoulder clod, pectoral meat, and mock tender were observed (0.13, 0.07, and 0.04%, respectively). Yield changes for subprimal brisket, plate, and flank were limited to increased ( < 0.01) proportion of flank steak and elephant ear (cutaneous trunci), 0.07 and 0.04%, respectively. Feeding duration notably altered ( = 0.01) weights and percentages of all subprimals except the brisket. Saleable yield increased ( = 0.01) by 0.192 kg/d with additional DOF. Moreover, trimmable fat and bone increased ( = 0.01) by 0.146 and 0.050 kg/d, respectively. These data illustrate improved saleable meat yields for calf-fed Holstein steers supplemented with ZH and provide the beef industry knowledge of fabrication yield changes throughout a wide range of harvest endpoints.
The effects of subunit composition on the inhibition of nicotinic receptors by the amphipathic blocker 2,2,6,6-tetramethylpiperidin-4-yl heptanoate.[Pubmed:15761116]
Mol Pharmacol. 2005 Jun;67(6):1977-90.
The therapeutic targeting of nicotinic receptors in the brain will benefit from the identification of drugs that may be selective for their ability to activate or inhibit a limited range of nicotine acetylcholine receptor subtypes. In the present study, we describe the effects of 2,2,6,6-tetramethylpiperidin-4-yl heptanoate (TMPH), a novel compound that is a potent inhibitor of neuronal nicotinic receptors. Evaluation of nicotinic acetylcholine receptor (nAChR) subunits expressed in Xenopus laevis oocytes indicated that TMPH can produce a potent and long-lasting inhibition of neuronal nAChR formed by the pairwise combination of the most abundant neuronal alpha (i.e., alpha3 and alpha4) and beta subunits (beta2 and beta4), with relatively little effect, because of rapid reversibility of inhibition, on muscle-type (alpha1beta1gammadelta) or alpha7 receptors. However, the inhibition of neuronal beta subunit-containing receptors was also decreased if any of the nonessential subunits alpha5, alpha6, or beta3 were coexpressed. This decrease in inhibition is shown to be associated with a single amino acid present in the second transmembrane domain of these subunits. Our data indicate great potential utility for TMPH to help relate the diverse central nervous system effects to specific nAChR subtypes.