Nesiritide (acetate)
目录号 : GC49301
A natriuretic peptide
Cas No.:1684439-46-0
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Nesiritide is a 32-amino acid natriuretic peptide and recombinant form of human brain natriuretic peptide .1 It increases ex vivo vasorelaxation induced by the calcium ionophore A23187 in porcine hearts isolated from a model of acute coronary occlusion when administered as a 2 µg/kg bolus dose followed by 0.01 µg/kg per minute infusion.2 Formulations containing nesiritide have previously been used in the treatment of congestive heart failure.
1.Hobbs, R.E., and Mills, R.M.Therapeutic potential of nesiritide (recombinant b-type natriuretic peptide) in the treatment of heart failureExpert Opin. Investig. Drugs8(7)1063-1072(1999) 2.Lazar, H.L., Bao, Y., Siwik, D., et al.Nesiritide enhances myocardial protection during the revascularization of acutely ischemic myocardiumJ. Card. Surg.24(5)600-605(2009)
| Cas No. | 1684439-46-0 | SDF | |
| Canonical SMILES | CC(O)=O.O=C(N1CCC[C@H]1C(N[C@@H](CCCCN[H])C(N[C@@H](CCSC)C(N[C@@H](C(C)C)C(N[C@@H](CCC(N)=O)C(NCC(N[C@@H](CO)C(NCC(N[C@@H](CSSC[C@H](N2)C(N[C@@H](CCCCN[H])C(N[C@@H](C(C)C)C(N[C@H](C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCNC(N)=N)C(N[C@@H](CC3=CNC=N3)C(O)=O)=O)=O)=O)CC(C)C)=O)=O)=O)C(N[C@H](C(NCC(N[C@@H](CCCNC(N)=N)C(N[C@@H](CCCCN[H])C(N[C@@H](CCSC)C(N[C@@H](CC(O)=O)C(N[C@@H](CCCNC(N)=N)C(N[C@@](C(N[C@@H](CO)C(N[C@@H](CO)C(N[C@@H](CO)C(N[C@@H](CO)C(NCC(N[C@H](C(NCC2=O)=O)CC(C)C)=O)=O)=O)=O)=O)=O)([H])[C@@H](C)CC)=O)=O)=O)=O)=O)=O)=O)CC4=CC=CC=C4)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@H](CO)N[H] | ||
| 分子式 | C143H244N50O42S4·C2H4O2 | 分子量 | 3524.1 |
| 溶解度 | Water: soluble | 储存条件 | -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 | 0.2838 mL | 1.4188 mL | 2.8376 mL |
| 5 mM | 0.0568 mL | 0.2838 mL | 0.5675 mL |
| 10 mM | 0.0284 mL | 0.1419 mL | 0.2838 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。
Restoration of cardiac metabolic flexibility by acetate in high-fat diet-induced obesity is independent of ANP/BNP modulation
Can J Physiol Pharmacol 2022 Jun 1;100(6):509-520.PMID:35395159DOI:10.1139/cjpp-2021-0531.
The present study hypothesized that cardiac metabolic inflexibility is dependent on cardiac atrial natriuretic peptide/brain natriuretic peptide (ANP/BNP) alteration and histone deacetylase (HDAC) activity. We further sought to investigate the therapeutic potential of short-chain amino acid (SCFA) acetate in high-fat diet (HFD)-induced obese rat model. Adult male Wistar rats were assigned into groups (n = 6 per group): Control, Obese, and Sodium acetate (NaAc)-treated and Obese + NaAc-treated groups received distilled water once daily (oral gavage), 40% HFD ad libitum, 200 mg/kg NaAc once daily (oral gavage), and 40% HFD + NaAc, respectively. The treatments lasted for 12 weeks. HFD resulted in increased food intake, body weight, and cardiac mass. It also caused insulin resistance and enhanced β-cell function, increased fasting insulin, lactate, plasma and cardiac triglyceride, total cholesterol, lipid peroxidation, tumor necrosis factor-α, interleukin-6, HDAC, and cardiac troponin T and γ-glutamyl transferase, and decreased plasma and cardiac glutathione with unaltered cardiac ANP and BNP. However, these alterations were averted when treated with acetate. Taken together, these results indicate that obesity induces defective cardiac metabolic flexibility, which is accompanied by an elevated level of HDAC and not ANP/BNP alteration. The results also suggest that acetate ameliorates obesity-induced cardiac metabolic inflexibility by suppression of HDAC and independent of ANP/BNP modulation.
Association of Biomarkers with Serious Cardiac Adverse Events during Abiraterone acetate Treatment in Castration Resistant Prostate Cancer
Transl Oncol 2016 Dec;9(6):600-605.PMID:27916295DOI:10.1016/j.tranon.2016.08.001.
Background: Abiraterone acetate is an effective drug for castration-resistant prostate cancer, but cardiac serious adverse events (SAEs) may occur. We studied their association with N-terminal pro-brain natriuretic peptide (NT-proBNP) and troponin T (TnT) during abiraterone therapy. Patients and methods: In a single institution, 17 patients were treated with abiraterone acetate 1 g daily with concomitant prednisone and then switched to dexametasone plus canrenone. Blood samples for PSA, NT-proBNP, and TnT were obtained at baseline and after 1, 3, and 6 months. Results: Five patients (29.4%) experienced G3 to 4 cardiac SAEs after a median of 13 weeks (range, 9-32), including pulmonary edema, heart failure, acute coronary syndrome, sinus bradycardia with syncope, and pulmonary edema. At baseline, 4 weeks, and 3 months, median NT-proBNP and TnT levels were higher in patients with subsequent cardiac SAEs (P= .03 and P= .04 for NT-proBNP and TnT at 3 months, respectively). After switching to dexametasone and introducing canrenone, no additional cardiac SAEs were noted. Overall response rate was 67%. Conclusions: Our study suggests a higher than expected risk of cardiac SAEs during abiraterone treatment which may well be due to the small sample size and the unrestricted entry criteria. However, baseline and frequent NT-proBNP and TnT monitoring predicted a higher risk for cardiac SAE. Larger studies should confirm our findings.
Effect of Testosterone on Natriuretic Peptide Levels
J Am Coll Cardiol 2019 Mar 26;73(11):1288-1296.PMID:30898204DOI:10.1016/j.jacc.2018.12.062.
Background: Circulating natriuretic peptide (NP) levels are markedly lower in healthy men than women. A relative NP deficiency in men could contribute to their higher risk of hypertension and cardiovascular disease. Epidemiological studies suggest testosterone may contribute to sex-specific NP differences. Objectives: This study aimed to determine the effect of testosterone administration on NP levels using a randomized, placebo-controlled design. Methods: One hundred and fifty-one healthy men (20 to 50 years of age) received goserelin acetate to suppress endogenous production of gonadal steroids, and anastrazole to suppress conversion of testosterone to estradiol. Subjects were randomized to placebo gel or 4 different doses of testosterone (1%) gel for 12 weeks. Serum N-terminal-pro-B-type natriuretic peptide (NT-proBNP) and total testosterone levels were measured at baseline and follow-up. Results: Men who did not receive testosterone replacement (placebo gel group) after suppression of endogenous gonadal steroid production experienced a profound decrease in serum testosterone (median 540 to 36 ng/dl; p < 0.0001). This was accompanied by an increase in median NT-proBNP (+8 pg/ml; p = 0.02). Each 1-g increase in testosterone dose was associated with a 4.3% lower NT-proBNP at follow-up (95% confidence interval: -7.9% to -0.45%; p = 0.029). An individual whose serum testosterone decreased by 500 ng/dl had a 26% higher predicted follow-up NT-proBNP than someone whose serum testosterone remained constant. Conclusions: Suppression of testosterone production in men led to increases in circulating NT-proBNP, which were attenuated by testosterone replacement. Inhibition of NP production by testosterone may partly explain the lower NP levels in men. (Dose-Response of Gonadal Steroids and Bone Turnover in Men; NCT00114114).
Co-exposure subacute toxicity of silica nanoparticles and lead acetate on cardiovascular system
Int J Nanomedicine 2018 Nov 21;13:7819-7834.PMID:30538461DOI:10.2147/IJN.S185259.
Background: The harmful effects following the release of nanomaterials into environment are of great concern today. Purpose: In this study, subacute effect due to co-exposure to low-dose silica nanoparticles (SiNPs) and lead acetate (Pb) on cardiovascular system was detected in Sprague Dawley male rats. Materials and methods: Histopathological and ultrastructural changes of heart, aortic arch and abdominal aorta were detected. Blood routine and blood biochemistry examinations were used to show the changes of blood components. The fibrinolytic and plasmin factors, inflammation-related factors and myocardial-related enzyme in serum were analysised by ELISA and Western blot assay. Results: Histopathological and ultrastructural examination of heart, aortic arch, and abdominal aorta showed that serious damage occurred in co-exposure group (n=6/group). Blood routine examination showed that leukocytosis and thrombocytopenia increased markedly, while changes in the erythrocyte count were not obvious in the co-exposure group. The expression of alanine transaminase (ALT) decreased obviously in co-exposure group, while no significant changes were noted in the expression of aspartate aminotransferase (AST), cholesterol (CHO), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), and low-density lipoprotein-cholesterol (LDL-C) in the co-exposure group on blood biochemistry analysis. In addition, data from ELISA analysis showed that the levels of fibrinolytic and plasmin factors, including thrombin time (TT), prothrombin time (PT), activated partial thromboplastin time (APTT), tissue-type plasminogen activator (t-PA), tissue factor pathway inhibitor (TFPI), and antithrombin III (AT III), were decreased, while those of human fibrinogen (FIB) and D-dimer (D2D) increased significantly in the co-exposure group. Moreover, the myocardial-related enzyme in serum, tested by ELISA, and cardiovascular-related protein expression of atrial natriuretic peptide and brain natriuretic peptide, tested by Western blot assay, was increased in the heart. Furthermore, the expression of inflammation factors such as C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) was increased in heart tissue subjected to combined exposure, which was manifested by Western blot assay, while the protein levels of angiotensin II (ANG II) and endothelin 1 were (ET-1) elevated in blood vessels in the co-exposure group. Conclusion: In conclusion, the major interactions involved in subacute toxicity due to co-exposure to low doses of SiNPs and Pb on cardiovascular system were expected to be additive and synergistic in nature. Co-exposure to SiNPs and Pb could aggravate the cardiovascular toxicity via endothelial damage, hypercoagulation, and cardiac injury in vivo.
Gateways to clinical trials
Methods Find Exp Clin Pharmacol 2004 May;26(4):295-318.PMID:15319808doi
Gateways to Clinical Trials is a guide to the most recent clinical trials in current literature and congresses. The data in the following tables has been retrieved from the Clinical Studies Knowledge Area of Prous Science Integrity, the drug discovery and development portal, http://integrity.prous.com. This issue focuses on the following selection of drugs: 166Ho-DOTMP 5A8; A-179578, abetimus sodium, adefovir dipivoxil, AGI-1067, AIDSVAX gp120 B/B, AK-602, alefacept alemtuzumab, aliskiren fumarate, ALVAC vCP1433, ALVAC vCP1452, anecortave acetate, arzoxifene hydrochloride, atazanavir sulfate, atlizumab, avasimibe; Binodenoson, BMS-488043; Choriogonadotropin alfa, ciclesonide, COL-1621, CVT-3146, CVT-E002, Cypher; Daptomycin, darbepoetin alfa, darunavir, D-D4FC, deferasirox, desloratadine, desmoteplase, duloxetine hydrochloride, DX-9065a; E-5564, efalizumab, emfilermin, emivirine, emtricitabine, enfuvirtide, estradiol acetate, ezetimibe; Frovatriptan; Gallium maltolate, gefitinib; HIV-1 Immunogen, human insulin; Iguratimod, IL-4/IL-13 Trap, imatinib mesylate, inhaled insulin, insulin glargine, irofulven, ISS-1018, ivabradine hydrochloride; Lutropin alfa; Melatonin; Nesiritide; O6-Benzylguanine, omapatrilat, oritavancin, ospemifene; Parecoxib sodium, peginterferon alfa-2a, pexelizumab, pimecrolimus, pirfenidone, pramlintide acetate, prasterone sulfate PT-141; Rasburicase, razaxaban hydrochloride, recombinant malaria vaccine, rhBMP-2/ACS, roflumilast, rosiglitazone maleate/metformin hydrochloride, rotavirus vaccine; SCH-D, sitaxsentan sodium, solifenacin succinate; Targinine hydrochloride, taxus, TER-199, tramadol hydrochloride/acetaminophen; Valdecoxib, valganciclovir hydrochloride, vatalanib succinate, VEG Trap(R1R2); Ximelagatran; Yttrium Y90 Epratuzumab.