Setipafant (BN-50727)
(Synonyms: 司替帕泛; BN-50727; LAU-0901) 目录号 : GC32559
Setipafant (BN-50727) 是一种血小板活化因子 (PAF) 拮抗剂。
Cas No.:132418-35-0
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Animal experiment: | Piglets[1] Male and female newborn piglets weighing 1550±31 g are used in all experiments. Six groups are studied. Group U4 is the nonsurgical control group (n=15). No anesthesia is given. Animals are entrusted to their mother and killed at D4. Group S is the sham control group (n=15). At D2 animals undergo laparotomy, intestinal exteriorization, and manipulation for 10 minutes before reintroduction to the abdominal cavity. They are killed at D4. Group I4 consist of animals (n=15) in which ischemia surgery is performed at D2, and animals are killed at D4. Group IT4 consist of animals (n=15) treated as in I4 together with treatment with Setipafant (BN 50727), a PAF receptor antagonist, orally (50 mg/kg of body weight) the day before and daily after surgery until death, and intraperitoneally (50 mg/kg) during surgery. Group I9 consisted of animals (n=15) in which ischemia surgery is performed at D2, and animals are killed at D9. Group IT9 consist of animals (n=15) undergoing the same procedure as in Is together with treatment with Setipafant as in IT4. Another group, U9, is made up of control animals (n=15) that are used only for weight and blood sample studies at D9. Rats[2] Male, Wistar rats weighing 160-205 g are used. Between 09 h 00 min and 10 h 00 min each day the animals are given an intraperitoneal injection of the PAF receptor antagonists, BN 52021 (10 mg/kg) or BN 50727(1 mg/kg), or their vehicle, and 30 min later they receive a subcutaneous injection of Dexamethasone sodium phosphate or vehicle. The effectiveness of BN 52021 and BN 50727 treatments is tested in preliminary experiments in anaesthetized (Inactin, 100 mg/kg, i.p.) male rats by injecting 25 and 50 ng/kg PAF into the right femoral vein 30 min before and 30 min after administration of either BN 52021, 10 mg/kg, i.p., or BN 50727, 1 mg/kg, i.p. Mean arterial blood pressure is monitored through a catheter inserted into the right femoral artery by an electromanometer using a Statham P23 dB pressure transducer. |
References: [1]. de Boissieu D, et al. Effect of BN 50727 on pathological findings and tissue platelet activating factor levels during ileal ischemia in newborn piglets. J Pediatr Surg. 1996 Dec;31(12):1675-9. | |
Setipafant is a platelet-activating factor (PAF) antagonist.
Animals are separated into six groups: U4, controls; S, sham operated animals undergoing laparotomy; I4 and I9, ligation of the mesenteric vessels in the last ileal loop; IT4 and IT9, same procedure together with treatment with Setipafant (50 mg/kg) orally before and after surgery and intraperitoneally during surgery. Animals are killed at day 4 in groups U4, S, I4 and IT4 and at day 9 in groups I9 and IT9, with histological studies and mediator measurements taken. Macroscopic and histological lesions of intestinal wall in groups I4, I9, IT4 and IT9 are similar to those of human neonatal necrotizing enterocolitis and do not vary according to the absence or the presence of Setipafant (BN 50727) treatment. Peritoneal bands are significantly reduced in treated groups IT4 and IT9 as compared with untreated ones I4 and I9. Mucosal PAF levels in the terminal ileum are higher in group I4 than in groups U4 or I9. In the upper loop, mucosal PAF levels are comparable in all groups. An increase in stool PAF levels is observed only in group I9, whereas values comparable to those observed in controls are detected in other groups[1]. Pretreatment of the animals with one or other of the structurally unrelated PAF receptor antagonists, BN 52021 (10 mg/kg, i.p.) or BN 50727 (1 mg/kg, i.p.) significantly reduces Dexamethasone-induced gastric damage. In these animals neither petechiae nor erosions are observed[2].
[1]. de Boissieu D, et al. Effect of BN 50727 on pathological findings and tissue platelet activating factor levels during ileal ischemia in newborn piglets. J Pediatr Surg. 1996 Dec;31(12):1675-9. [2]. Filep JG, et al. Dexamethasone-induced gastric mucosal damage in the rat: possible role of platelet-activating factor. Br J Pharmacol. 1992 Apr;105(4):912-8.
| Cas No. | 132418-35-0 | SDF | |
| 别名 | 司替帕泛; BN-50727; LAU-0901 | ||
| Canonical SMILES | O=C(N(C1)CCC2=C1SC3=C2C(C4=CC=CC=C4Cl)=NCC5=NN=C(C)N53)NC6=CC=C(OC)C=C6 | ||
| 分子式 | C26H23ClN6O2S | 分子量 | 519.02 |
| 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.9267 mL | 9.6335 mL | 19.2671 mL |
| 5 mM | 0.3853 mL | 1.9267 mL | 3.8534 mL |
| 10 mM | 0.1927 mL | 0.9634 mL | 1.9267 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 | ||||||||||
| 计算重置 | ||||||||||
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。
Determination of the anti-platelet-activating factor BN-50727 and metabolites in human urine by high-performance liquid chromatography using solid-phase extraction
J Chromatogr B Biomed Appl 1996 Mar 3;677(2):388-92.PMID:8704947DOI:10.1016/0378-4347(95)00481-5.
A sensitive and selective HPLC solid-phase extraction procedure was developed for the determination of platelet-activating factor antagonist BN-50727 and its metabolites in human urine. The procedure consisted in a double solid-phase extraction of the urine samples on cyanopropyl and silica cartridges, followed by an automated solid-phase extraction of the drug and metabolites on CBA cartridges and posterior elution on-line to the chromatographic system for its separation. The method allowed quantitation in the concentration range 10-2400 ng/ml urine for both BN-50727 and the main metabolite, the O-demethylated BN-50727 product. The limit of quantitation for both compounds was 10 ng/ml. The inter-assay precision of the method, expressed as relative standard deviation, ranged from 1.9 to 4.5% for BN-50727 and from 2.5 to 9.0% for the metabolite. The accuracy, expressed as relative error, ranged from -2.4 to 4.2% and from 0.2 to 6.2%, respectively. This paper describes the validation of the analytical methodology for the determination of BN-50727 in human urine and also for its metabolites. The method has been used to follow the time course of BN-50727 and its metabolites in human urine after single-dose administration.
Determination of the anti-platelet-activating factor BN-50727 and its metabolites in human plasma by high-performance liquid chromatography-solid-phase extraction
J Chromatogr B Biomed Appl 1995 Jun 23;668(2):281-90.PMID:7581863DOI:10.1016/0378-4347(95)00085-w.
A sensitive and selective HPLC-solid-phase extraction procedure was developed for the determination of platelet-activating factor antagonist BN-50727 and its metabolites in human plasma. The procedure consisted of an automated solid-phase extraction of the drug and metabolites on disposable propylcarboxylic acid cartridges, followed by on-line chromatographic separation. The method was linear from 3.75 to 2400 ng/ml and the limit of quantitation for BN-50727 in plasma samples was 3.75 ng/ml. The within-run precision of the method, expressed as relative standard deviation, ranged from 2.1 to 8.1%. The accuracy, expressed as relative error, ranged from -3.5 to 4.0%. For the main metabolite, the O-demethylated BN-50727 product, the method was linear from 7.5 to 2400 ng/ml and the limit of quantitation in plasma was 7.5 ng/ml. The within-run precision ranged from 2.1 to 11.0% and the accuracy from -5.3 to 1.1%. This paper describes the validation of the analytical methodology for the determination of BN-50727 in human plasma and also of its metabolites. The method has been used to follow the time course of BN-50727 and its metabolites in human plasma after administration of single and multiple doses.
Platelet-activating factor stimulates gastric acid secretion in isolated rabbit gastric glands
Am J Physiol 1995 Jun;268(6 Pt 1):G889-94.PMID:7611410DOI:10.1152/ajpgi.1995.268.6.G889.
We examined the effect of platelet-activating factor (PAF) on gastric acid secretion by isolated rabbit gastric glands as determined by [14C]aminopyrine ([14C]AP) uptake. PAF, histamine, and carbachol time- and concentration-dependently stimulated [14C]AP uptake, with estimated half-maximal effective concentrations of 60 pM, 0.25 microM, and 0.1 microM, respectively. PAF-induced [14C]AP uptake was inhibited by the specific PAF antagonists BN-50727 and SR-27417 and by the proton pump inhibitors omeprazole and lansoprazole. However, the H2-receptor antagonist famotidine had no effect. Buffering extracellular Ca2+ by ethylene glycol-bis(beta-amino-ethyl ether)-N,N,N',N'-tetraacetic acid resulted in a shift to the right of the time-course effect of PAF without altering the maximal response, whereas buffering intracellular Ca2+ by 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid 2-acetoxymethyl ester, as well as blocking Ca2+ channels by verapamil, inhibited PAF-induced [14C]AP uptake. Intracellular Ca2+ concentration in isolated rabbit gastric glands, as measured by fura 2-acetoxymethyl ester, concentration-dependently increased in response to PAF, to a maximum of 1.5-fold for 0.1 microM. These results suggest that PAF stimulates gastric acid secretion via specific receptors activating intracellular Ca2+ mobilization, which could be located on the parietal cells.