Xipamide
(Synonyms: 希伯胺) 目录号 : GC39517
Xipamide is a sulfonamide-based diuretic as well as a saluretic with antihypertensive activity.
Cas No.:14293-44-8
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
Xipamide is a sulfonamide-based diuretic as well as a saluretic with antihypertensive activity.
| Cas No. | 14293-44-8 | SDF | |
| 别名 | 希伯胺 | ||
| Canonical SMILES | O=C(NC1=C(C)C=CC=C1C)C2=CC(S(=O)(N)=O)=C(Cl)C=C2O | ||
| 分子式 | C15H15ClN2O4S | 分子量 | 354.81 |
| 溶解度 | DMSO: 250 mg/mL (704.60 mM) | 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 | 2.8184 mL | 14.092 mL | 28.1841 mL |
| 5 mM | 0.5637 mL | 2.8184 mL | 5.6368 mL |
| 10 mM | 0.2818 mL | 1.4092 mL | 2.8184 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 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 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
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计算结果:
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。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Xipamide. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy
Drugs 1985 Oct;30(4):313-32.PMID:3905333DOI:10.2165/00003495-198530040-00002.
Xipamide is a diuretic derived from salicylic acid and has a structural resemblance to chlorthalidone. Its pharmacodynamic profile shows a diuretic efficacy is similar to that of frusemide (furosemide) at doses up to 40 mg, but the onset and duration of action are comparable to those of hydrochlorothiazide. Xipamide has been studied mostly in the treatment of mild to moderate essential hypertension, with few controlled studies of its use in oedematous states. The efficacy of Xipamide 20 to 40 mg once daily in patients with mild to moderate hypertension is comparable to that of bendrofluazide 5 mg, bumetanide 1 mg or hydrochlorothiazide 50 mg when used alone in newly treated or previously treated patients. The addition of Xipamide 20 to 40 mg daily to regimens containing beta-blockers, adrenergic neuron-blocking drugs and/or methyldopa has resulted in a further reduction in blood pressure. A few studies in oedematous states suggest that Xipamide 40 to 80 mg is comparable in efficacy to equal doses of frusemide, and that the side effects of hypokalaemia, hyperuricaemia and increased blood glucose in diabetics or latent diabetics are similar to those of other diuretics. Thus, Xipamide is a suitable alternative to other diuretics in the treatment of mild to moderate hypertension and combines the efficacy of frusemide with a less abrupt action in the treatment of oedema.
Xipamide and cyclopenthiazide in essential hypertension--comparative effects on blood pressure and plasma potassium
Br J Clin Pharmacol 1982 Jun;13(6):859-63.PMID:7046777DOI:10.1111/j.1365-2125.1982.tb01879.x.
1 The blood pressure lowering effect of Xipamide, a non-thiazide diuretic given for 6 weeks was compared in a randomised cross-over trial with that of cyclopenthiazide in 14 patients with essential hypertension. 2 Xipamide 10 or 20 mg given once daily was as effective in lowering supine blood pressure as daily cyclopenthiazide 0.5 mg. There was no difference in the blood pressure lowering effect of 10 mg Xipamide daily for 2 weeks compared to 20 mg daily given for a further 4 weeks. 3 Plasma potassium was reduced by both drugs, but markedly more after both 10 mg and 20 mg Xipamide than after cyclopenthiazide 0.5 mg. By the sixth week of treatment 13 of 14 patients on Xipamide but only 6 of 14 on cyclopenthiazide has plasma potassium concentrations of, or less than, 3.5 mmol/l. The fall in plasma potassium was significantly greater and the final plasma potassium concentration was significantly lower after either dose of Xipamide than after cyclopenthiazide. 4 These results suggest that 10 mg or 20 mg of Xipamide daily is effective in lowering blood pressure in hypertensive patients but is associated with hypokalaemia. In view of recent evidence linking diuretic-induced hypokalaemia with cardiac dysrhythmias in patients with essential hypertension we would suggest that thiazide diuretics be used in preference to Xipamide for the routine management of essential hypertension. Our results also suggest that the currently recommended dose of Xipamide (20 mg) for the treatment of hypertension is excessive, and lower amounts than 10 mg per day might possibly be as effective in lowering blood pressure with less adverse metabolic consequences.
Inhibition by Xipamide of amiloride-induced acidification in cultured rat cardiocytes
Eur J Pharmacol 1997 Apr 18;324(2-3):289-94.PMID:9145785DOI:10.1016/s0014-2999(97)00087-3.
The diuretic drug Xipamide improves myocardial relaxation in hypertensive patients with left ventricular hypertrophy, but its mechanism of action is unknown. Here, Xipamide was tested in cultured rat heart myogenic H9c2 cells and newborn cardiomyocytes for its effects on cell acidification (and Ca2+ mobilization). In H9c2 cells, blocking Na+/H+ exchange with amiloride (2 mM) provoked cell acidification with rate = 0.82 +/- 0.17 pH units/h (n = 6). Xipamide 1 microM maximally inhibited 50 +/- 7% (n = 9) of cell acidification. The action of Xipamide required the presence of HCO3- and was antagonized by the HCO3(-)-transport blocker DIDS (4,4'-diisothiocyanostilbene-2.2'-disulfonic acid). Conversely, the carbonic anhydrase (EC 4.2.1.1) inhibitor acetazolamide failed to prevent Xipamide action. Finally, Xipamide was without significant effect on the Ca2+ signals induced by endothelin-1, vasopressin or the Ca2+ ionophore ionomycin. In newborn rat cardiomyocytes, Xipamide reduced amiloride-induced cell acidification at similar concentrations as in H9c2 cardiocytes, but with a slightly higher extent of maximal inhibition (70-80%). In conclusion, Xipamide reduced amiloride-dependent cell acidification in the rat heart myogenic H9c2 cell line and in newborn rat cultured cardiomyocytes. This action of Xipamide seems to be related to a complex interaction with DIDS-sensitive HCO3- movements. Prevention of cell acidification by Xipamide could be involved in the beneficial effects of this compound in myocardial relaxation and left ventricle filling in hypertensive patients with left ventricular hypertrophy.
[Beneficial effects of Xipamide on pH and Ca2+ ions of cardiac cells]
Arch Mal Coeur Vaiss 1990 Jul;83(8):1271-4.PMID:2124467doi
We have shown that Xipamide is the only antihypertensive agent able to selectively inhibit the anion exchanger (AE), a transport system translocating (i) chloride and bicarbonate (thus participating to internal pH), but also (ii) Na+ as NaCO3-(which could explain the natriuretic effect of Xipamide). On the other hand, Ollivier (Val de Grâce, Paris) has shown that Xipamide exerts a beneficial action on heart by favoring left ventricular relaxation in essential hypertensive patients exhibiting cardiac hypertrophy. In order to understand this clinical effect, we have studied the effect of Xipamide on pH and cytosolic free calcium in cultured Rat cardiocytes (H9c2 line). pHi was measured at equilibrium using 14C-DMO and cytosolic free calcium was measured spectrofluorimetrically with Fura2 (Shimadzu RF 5000). 1) The presence of bicarbonate induced a 0.39 +/- 0.14 (mean +/- SD; n = 3) alkalinization; final pHi was 7.08 +/- 0.15 (n = 8). Nor 20 microM DIDS (specific AE inhibitor), neither 50 microM Xipamide were able to modify this result. This suggests that the alkalinization is not due to the anion exchanger. 2) After preincubation in the presence of 0.5 microM DIDS, we observed a 0.35 +/- 0.21 acidification (n = 4). Conversely, 0.5 microM Xipamide induced a 0.22 +/- 0.16 alkalinization (n = 4). 3) Xipamide (0.5-500 microM) increased the internal K/Na ratio (at 0.5 microM, delta = 3.1 +/- 0.2; n = 3); this was mainly due to internal K+ increase.(ABSTRACT TRUNCATED AT 250 WORDS)
Pharmacodynamics and pharmacokinetics of Xipamide in patients with normal and impaired kidney function
Eur J Clin Pharmacol 1984;26(4):513-20.PMID:6734710DOI:10.1007/BF00542150.
The effect of a single oral dose of 40 mg Xipamide on urinary excretion of Na+, K+, Cl-, Ca2+ and Mg2+ in healthy subjects and in patients with varying degrees of renal impairment was compared with various conventional diuretics. Xipamide caused marked excretion of Na+ and Cl-, whereas the diuretic produced only moderate kaliuresis; urinary excretion of Ca2+ was increased in proportion to Na+, like the loop diuretics. Xipamide affected electrolyte excretion even in patients with a creatinine clearance below 30 ml/min, as do the loop diuretics, too. Therefore, the pharmacodynamic characteristics of Xipamide are more like those of a loop diuretic than of a thiazide. Xipamide was good bioavailable, its t 1/2 beta was 7 h and urinary recovery of the undegraded drug was 40% of the given dose. In renal insufficiency, t 1/2 beta increased from 7 to only 9h, yielding a moderate increase in the AUC. Urinary recovery of the drug was reduced in proportion to the reduction in the creatinine clearance of the patient. Therefore, significant extrarenal elimination of the diuretic must be postulated, which suffices to prevent significant drug accumulation in renal failure.