Tiapamil hydrochloride (Ro 11-1781)
(Synonyms: 噻帕米盐酸盐,Ro 11-1781) 目录号 : GC32549
Tiapamil hydrochloride (Ro 11-1781) 是一种钙通道阻滞剂。
Cas No.:57010-32-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Tiapamil hydrochloride is a calcium channel blocker.
Tiapamil, a new calcium antagonist: hemodynamic effects in patients with acute myocardial infarction. Tiapamil is a new verapamil congener.Without precipitating left ventricular failure, Tiapamil reduced afterload and heart rate and maintained cardiac index while apparently improving diastolic compliance[1]. Tiapamil, a new calcium channel blocking agent with anti-anginal efficacy[2].
[1]. Eichler HG, et al. Tiapamil, a new calcium antagonist: hemodynamic effects in patients with acute myocardial infarction. Circulation. 1985 Apr;71(4):779-86. [2]. Khurmi NS, et al. Tiapamil, a new calcium channel blocking agent for the treatment of effort induced chronic stableangina pectoris.
| Cas No. | 57010-32-9 | SDF | |
| 别名 | 噻帕米盐酸盐,Ro 11-1781 | ||
| Canonical SMILES | CN(CCC1=CC=C(OC)C(OC)=C1)CCCC(S(CCC2)(=O)=O)(C3=CC=C(OC)C(OC)=C3)S2(=O)=O.[H]Cl | ||
| 分子式 | C26H38ClNO8S2 | 分子量 | 592.16 |
| 溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.6887 mL | 8.4437 mL | 16.8873 mL |
| 5 mM | 0.3377 mL | 1.6887 mL | 3.3775 mL |
| 10 mM | 0.1689 mL | 0.8444 mL | 1.6887 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
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Cardiovascular effects of tiapamil (Ro 11-1781), a new calcium-entry blocker
J Cardiovasc Pharmacol 1982 May-Jun;4(3):419-29.PMID:6177938DOI:10.1097/00005344-198205000-00012.
We studied the hemodynamic effects of the new calcium antagonist tiapamil (Ro 11-1781) in anesthetized open-chest dogs and compared them with those of verapamil. Increasing doses of tiapamil injected intravenously caused the following hemodynamic effects: increase in coronary flow and decrease in coronary vascular resistance, followed by decreases in heart rate, blood pressure, and total peripheral resistance. Tiapamil did not depress myocardial contractility over a rather wide dose range, while verapamil did. Tiapamil was more effective in increasing coronary flow than verapamil. Cardiac autonomic denervation did not modify the tiapamil-induced decrease in coronary vascular resistance and did not cause tiapamil to display negative inotropism. Both tiapamil and verapamil reduced the extent of S-T segment elevation in the epicardial electrocardiogram produced by transient occlusion of the left anterior descending coronary artery. Neither drug had this effect when heart rate was kept constant by atrial pacing. In contrast to nitroglycerin, tiapamil dilated small but not large coronary arteries. Tiapamil raised PO2 relatively more in the subendocardial than in the subepicardial layers of the myocardium. The hemodynamic and electrocardiographic effects of tiapamil were not changed by diphenylhydantoin and disopyramide or by pindolol, a beta-adrenoceptor blocking agent with intrinsic sympathomimetic activity. However, the decreases in heart rate and blood pressure in response to propranolol were enhanced by tiapamil.
Bioelectrical and mechanical effects of tiapamil (Ro 11-1781) on isolated guinea pig myocardium
Cardiovasc Res 1986 Jan;20(1):42-51.PMID:3708640DOI:10.1093/cvr/20.1.42.
In isolated electrically stimulated guinea pig papillary muscles tiapamil exerts a negative inotropic action that corresponds to its presumptive inhibitory effects on the slow-channel-mediated transmembrane Ca2+ influx. However, contractile depression is always accompanied by marked alterations of the normal Na+-carried action potential. Thus Na+-dependent upstroke velocity (dV/dtmax) declines while the length of the plateau phase increases. These observations indicate that tiapamil, besides inhibiting Ca2+ inflow, also interferes with the fast inward Na+ current and possibly also reduces the repolarising K+ efflux. After partial depolarisation with a K+-rich tyrode solution (19 mmol X litre-1 K+). tiapamil lowers the Ca2+-dependent contractile force as it reduces the bioelectric parameters (upstroke velocity, amplitude, duration) of the Ca2+-mediated action potentials. Moreover, in partially depolarised myocardium, the Mg2+-induced bioelectric membrane activity is suppressed by tiapamil. Tiapamil probably operates as an agent with mixed Na+-, K+-, Ca2+- and Mg2+-antagonistic effects and, in this respect, differs considerably from the more specific Ca2+ antagonists such as verapamil, D 600 (gallopamil), nifedipine (and other 1,4-dihydropyridines) or diltiazem. However, tiapamil by virtue of its combined damping actions on both transmembrane Na+ and Ca2+ conductivities (together with prolongation of the action potential plateau), is a drug which exerts, simultaneously, the fundamental myocardial membrane effects of antiarrhythmic agents of group I, III and IV, according to the classification of Singh and Vaughan Williams. Thus these bioelectrical observations are in accordance with the results of clinical studies on tiapamil, which have demonstrated directly its antiarrhythmic efficacy.
Antihypertensive properties of tiapamil (Ro 11-1781)--a new calcium antagonist--in patients with mild and moderate essential hypertension
Int J Clin Pharmacol Res 1987;7(6):443-54.PMID:3440635doi
An open, non-comparative study, with a new calcium antagonist-tiapamil, was undertaken in 22 patients with mild and moderate essential hypertension (stage I-II WHO). After a two-week placebo period, patients were treated with tiapamil, 300-600 mg twice daily during a period of six weeks (Dose-finding period). Thereafter patients were continued on tiapamil during a 54 week period (Long-term follow-up). In some patients it was necessary to add the diuretic hydrochlorothiazide to obtain adequate control of the arterial hypertension. Monotherapy with tiapamil normalized supine diastolic blood pressure after the first six weeks in 17 of the 21 evaluable patients, and reduced it by greater than or equal to 10 mmHg (1.3 kPa) from baseline without normalization in two patients. In the two remaining cases the decrease was less than 10 mmHg. The optimal dose administered at six weeks in those patients who responded to treatment (normalization or decrease by greater than or equal to 10 mmHg.) was 600 mg/day in 32% of the cases, 750-900 mg/day in 47% and more than 900 mg/day in 21%. After completion of the dose-finding part, 19 patients continued treatment for a further 54 weeks. In 16 out of 19 patients hydrochlorothiazide was added to enhance the antihypertensive effect. All three patients who received tiapamil monotherapy throughout the trial, had normalized supine diastolic blood pressure on completing the study. In the 16 patients with the combination therapy, the addition of hydrochlorothiazide led in two patients to no further decrease in supine diastolic blood pressure, to an additional decrease by less than 10 mmHg in ten patients and by greater than or equal to 10 mmHg in four in comparison with the values obtained before starting combination therapy. At the end of the study 11 of these 16 patients had normalized supine diastolic blood pressure. The mean daily dose was 900 +/- 45 mg of tiapamil and 39 +/- 4 mg of hydrochlorothiazide. Both monotherapy and the combination regimen were well tolerated, and no effects attributable to drug interactions were observed. It may be concluded that tiapamil in oral doses of 300-600 mg twice daily is an effective antihypertensive agent with an excellent tolerance when administered for a period of 54 weeks.
Antiarrhythmic effect of the calcium antagonist tiapamil (Ro 11-1781) by intravenous administration in patients with coronary heart disease
Clin Cardiol 1980 Dec;3(6):371-6.PMID:6161729DOI:10.1002/clc.4960030603.
Twenty coronary patients with a median age of 76 years were treated in the coronary care unit with tiapamil, a new Ca2+ antagonist, by intravenous infusion (until December, 1979, the generic name was dimeditiapramine). The following arrhythmias were identified: atrial fibrillation with ventricular rate greater than 95 beats/min (5 patients); supraventricular premature complexes (SVPC) (4 patients); and ventricular premature complexes (VPC), Lown grades 2-4 (15 patients). Electrocardiograms and hemodynamic parameters were continuously monitored prior to, during, and after the therapy. In patients with atrial fibrillation, sinus rhythm was not restored, but tiapamil decreased the ventricular rate by 54%. In patients with VPC, the median frequency of VPC decreased from 310.5 before tiapamil to 32.5 beats/h at the fourth hour of therapy (p less than 0.01). The median ectopic/sinus beat ratio decreased from 0.083 (pretreatment) to 0.008 at the fourth hour of infusion (p less than 0.10). In one of the patient with an insufficient decrease in the number of VPC, the VPOC changed from class 4a (pretreatment) to class 2 (during the therapy), returning to class 4a after the infusion was stopped. Tiapamil reduced the median systolic and diastolic blood pressures by 8.3 and 7.1%, respectively (p less than 0.05), the third hour. Hypotension and bradycardia were observed in 5/20 patients. The results show that tiapamil is effective against both supraventricular and ventricular arrhythmias, and thus its spectrum of action differs from that of other calcium antagonists.
Tiapamil, Ro 11-1781, a Ca++ antagonist. An improved synthesis, physiochemical properties, preparation of a deuterated derivative
Cardiology 1982;69 Suppl:26-30.PMID:7151082DOI:10.1159/000173536.
An improved synthesis of tiapamil 3, Ro 11-1781, N-(3,4-dimethoxyphenethyl)-2-(3,4-dimethoxyphenyl)-N-methyl-m-dithiane-2- propylamine 1,1,3,3-tetraoxide is described. The structure of the corresponding hydrochloride monohydrate 4, a Ca++ antagonist has been confirmed by an X-ray crystallographic analysis. Since biotransformation of tiapamil into metabolites 5, 6 and 7 occurs mainly in the close vicinity of the nitrogen atom, compound 8 bearing seven deuterium atoms has been synthesised.