Isopropamide - CAS 7492-32-2
Catalog number: 7492-32-2
Category: Inhibitor
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Molecular Formula:
C23H33N2O
Molecular Weight:
353.52
COA:
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Targets:
Others
Description:
Isopropamide is a long-acting anticholinergic drug. It can be used for the treatment of peptic ulcers and other gastrointestinal disorders including hyperacidity and hypermotility. It is often provided as an iodide salt, but is also available as a bromide or chloride salt.
Purity:
98%
Appearance:
Powder
Synonyms:
(3-carbamoyl-3,3-diphenylpropyl)diisopropylmethylammonium;(3-Aminocarbonyl-3,3-diphenylpropyl)diisopropylmethylaminium;C07055
Solubility:
Soluble in DMSO
Storage:
-20℃ Freezer
MSDS:
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Application:
peptic ulcers and other gastrointestinal disorders
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Quantity:
Milligrams-Grams
InChIKey:
JTPUMZTWMWIVPA-UHFFFAOYSA-O
InChI:
1S/C23H32N2O/c1-18(2)25(5,19(3)4)17-16-23(22(24)26,20-12-8-6-9-13-20)21-14-10-7-11-15-21/h6-15,18-19H,16-17H2,1-5H3,(H-,24,26)/p+1
Canonical SMILES:
CC(C)[N+](C)(CCC(c1ccccc1)(c2ccccc2)C(=O)N)C(C)C
1.Muscarinic cholinergic activation of mouse spleen cells cytotoxic to tumor cells in vitro.
Lane MA J Natl Cancer Inst. 1978 Sep;61(3):923-6.
Carbamylcholine, acting via a pharmacologically specific receptor, had the ability to activate effector populations of spleen cells from female BALB/cfC3H and BALB/c mice; those cell populations were then significantly reactive in vitro against syngeneic tumor target cells but were only minimally reactive to normal syngeneic target tissues. The induced reactivity was inhibited by the muscarinic cholinergic antagonists atropine, scopolamine, and isopropamide, but not by the nicotinic antagonist d-tubocurare, and it appeared to involve both T-cell and non-T-cell effectors.
2.Competitive and non-competitive antagonism exhibited by 'selective' antagonists at atrial and ileal muscarinic receptor subtypes.
Eglen RM;Whiting RL Br J Pharmacol. 1987 Apr;90(4):701-7.
The affinity of a number of 'selective' agonists and antagonists has been assessed at atrial or ileal muscarinic receptors by use of in vitro functional analysis. The most selective compound for ileal muscarinic receptors was silabenzhexol (approx. 50 fold), and to a lesser extent benzhexol (approx. 5 fold). Conversely, the most selective compound for the atrial muscarinic receptors was AF-DX 116 (approx. 6 fold). The novel M1-receptor antagonist, telenzepine and other antagonists such as propantheline and isopropamide did not distinguish between atrial and ileal receptors. Dicyclomine, adiphenine, hexahydroadiphenine and oxyphenonium exhibited competitive antagonism at atrial receptors but non-competitive antagonism at ileal receptors. No conclusions could, therefore, be drawn with regard to their selectivity. The agonists, arecaidine propargyl ester (APE), ethoxyethyltriethylammonium (EOE) and carbachol, exhibited some selectivity in potency but little difference in affinity. It is concluded that the study supports the existence of ileal and atrial muscarinic receptor subtypes. However, the use of dicyclomine and related compounds in receptor classification is limited.
3.Effect of isopropamide on response to oral cimetidine in patients with Zollinger--Ellison syndrome.
McCarthy DM;Hyman PE Dig Dis Sci. 1982 Apr;27(4):353-9.
Patients with Zollinger-Ellison syndrome whose gastric acid secretion or symptoms were not controlled by cimetidine in conventional dosage were selected for studies of responsiveness of their acid secretion to increasing doses of cimetidine, used either alone or in combination with a long-acting anticholinergic agent, isopropamide iodide. Results indicate that in the group as a whole the suppression achieved with a 900-mg dose of cimetidine was not significantly better than that achieved with a 300-mg dose, although in individual cases this did not hold true. In individuals the combination of cimetidine and isopropamide was generally more effective in suppressing acid secretion than cimetidine alone, used either in the same dose as in the combination or in the next highest possible dosage. This was also true in the group as a whole, where combined therapy showed significant advantage over either drug alone in controlling acid secretion, in the third, fourth, and fifth hours following administration of the drugs. The data suggest that in the minority of patients not controlled by cimetidine 300-600 mg q6h per os, addition of isopropamide (20-40 mg/day) may be preferable to further increasing the dose of cimetidine.
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CAS 7492-32-2 Isopropamide

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