C-type natriuretic peptide (1-22) (human, rat, swine)
目录号 : GC12034
C 型钠尿肽 (1-22)（人、大鼠、猪）（C-type natriuretic peptide (1-22) (human, rat, swine) ）是一种存在于血浆和脑脊液中的内源性肽。
Cas No.:127869-51-6
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
| Cell experiment [1]: | |
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Cell lines |
CHO cells |
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Preparation Method |
To evaluate the human NPR (hNPR) agonist activities of the test compounds(C-type natriuretic peptide (1-22) (human, rat, swine)), Using Chinese hamster ovarian (CHO) cells stably expressing hNPR-A or hNPR-B. Each compound was added to the cells in duplicate and incubated for 15 min. Cells were lysed. |
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Reaction Conditions |
0.01-1000nM C-type natriuretic peptide (1-22) (human, rat, swine)for 15 min |
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Applications |
C-type natriuretic peptide (1-22) (human, rat, swine) increased cGMP production in CHO cells expressing human NPR-B in a concentration-dependent manner. |
| Animal experiment [1]: | |
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Animal models |
Sprague Dawley (SD) rats |
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Preparation Method |
Rats received C-type natriuretic peptide (1-22) (human, rat, swine) or ASB20123 by intravenous (iv) injection into the tail vein or subcutaneous (sc) injection into the back. |
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Dosage form |
C-type natriuretic peptide (1-22) (human, rat, swine) iv (20 nmol/kg) or sc (50 nmol/kg) |
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Applications |
C-type natriuretic peptide (1-22) (human, rat, swine) could be transported across the vascular wall and reach NPR-B in peripheral tissues. |
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References: [1].Morozumi N, Yotsumoto T, Yamaki A, Yoshikiyo K, Yoshida S, Nakamura R, Jindo T, Furuya M, Maeda H, Minamitake Y, Kangawa K. ASB20123: A novel C-type natriuretic peptide derivative for treatment of growth failure and dwarfism. PLoS One. 2019 Feb 22;14(2):e0212680. doi: 10.1371/journal.pone.0212680. PMID: 30794654; PMCID: PMC6386482. |
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C-type natriuretic peptide (1-22) (human, rat, swine) is an endogenous peptide found in plasma and cerebrospinal fluid[2]. C-type natriuretic peptide (CNP) is a member of the natriuretic peptide (NP) family [3]. It is also a potent, endothelial-derived relaxant and growth-inhibitory factor[6]. C-type natriuretic peptide (1-22) (human, rat, swine) is an agonist for the natriuretic peptide receptor NPR2 (NPRB) and has an affinity for NPR3 (NPRC). C-type natriuretic peptide (1-22) (human, rat, swine) can inhibit L-type calcium current in cardiomyocytes, has anti-proliferation effect in cardiac fibroblasts in vitro, and can promote vasodilation[7].
C-type natriuretic peptide (1-22) (human, rat, swine) increased cGMP production in CHO cells expressing human NPR-B in a concentration-dependent manner[1].
C-type natriuretic peptide (1-22) (human, rat, swine) could be transported across the vascular wall and reach NPR-B in peripheral tissues[1]. exogenous CNP(1-22) improved endochondral ossification and accelerated bone growth in mice after constant intravenous infusion at a large dose only[4]. I.c.v. administration of C-type natriuretic peptide (1-22) (human, rat, swine) in a dose of 2 nmol induced an increase in the severity of picrotoxin-kindled convulsions 24 and 48 hrs after application of the peptide[5].
References:
[1]. Morozumi N, Yotsumoto T, et,al. ASB20123: A novel C-type natriuretic peptide derivative for treatment of growth failure and dwarfism. PLoS One. 2019 Feb 22;14(2):e0212680. doi: 10.1371/journal.pone.0212680. PMID: 30794654; PMCID: PMC6386482.
[2]. Minamino N, Makino Y, et,al.Characterization of immunoreactive human C-type natriuretic peptide in brain and heart. Biochem Biophys Res Commun. 1991 Aug 30;179(1):535-42. doi: 10.1016/0006-291x(91)91404-z. PMID: 1831979.
[3]. Potter LR, Yoder AR, et,al. Natriuretic peptides: their structures, receptors, physiologic functions and therapeutic applications. Handb Exp Pharmacol. 2009;(191):341-66. doi: 10.1007/978-3-540-68964-5_15. PMID: 19089336; PMCID: PMC4855512.
[4]. Yasoda A, Kitamura H, et,al. Systemic administration of C-type natriuretic peptide as a novel therapeutic strategy for skeletal dysplasias. Endocrinology. 2009 Jul;150(7):3138-44. doi: 10.1210/en.2008-1676. Epub 2009 Mar 12. PMID: 19282381; PMCID: PMC2703521.
[5]. Mazarati AM, HalÁszi E, et,al. ANP(1-28), BNP(1-32) and CNP(1-22) increase the severity of picrotoxin-kindled seizure syndrome in rats. Life Sci. 1993;52(3):PL19-24. doi: 10.1016/0024-3205(93)90227-t. PMID: 8423706.
[6]. Buckley MG, Jenkins GH, et,al. Circulating C-type natriuretic peptide is increased in orthotopic cardiac transplant recipients and associated with cardiac allograft vasculopathy. Clin Sci (Lond). 2000 Nov;99(5):467-72. PMID: 11052928.
[7]. Pejchalova K, Krejci P, et,al.C-natriuretic peptide: an important regulator of cartilage. Mol Genet Metab. 2007 Nov;92(3):210-5. doi: 10.1016/j.ymgme.2007.06.014. Epub 2007 Aug 6. PMID: 17681481.
C 型钠尿肽 (1-22)（人、大鼠、猪）（C-type natriuretic peptide (1-22) (human, rat, swine) ）是一种存在于血浆和脑脊液中的内源性肽[2]。 C型利钠肽(CNP)是利钠肽(NP)家族[3]的一员。它还是一种有效的内皮衍生松弛剂和生长抑制因子[6]。 C-type natriuretic peptide (1-22) (human, rat, swine) 是利钠肽受体 NPR2 (NPRB) 的激动剂，对 NPR3 (NPRC) 具有亲和力。 C型钠尿肽（1-22）（人、大鼠、猪）可抑制心肌细胞L型钙电流，在体外对心肌成纤维细胞具有抗增殖作用，并可促进血管舒张[7].
C 型钠尿肽 (1-22)（人、大鼠、猪）以浓度依赖性方式增加表达人 NPR-B 的 CHO 细胞中 cGMP 的产生[1] .
C型钠尿肽（1-22）（人、大鼠、猪）可跨血管壁转运，到达外周组织的NPR-B[1] 。外源性 CNP(1-22) 仅在大剂量持续静脉输注后改善软骨内骨化并加速骨骼生长[4]。 I.c.v.施用 2 nmol 剂量的 C 型利钠肽 (1-22)（人、大鼠、猪）可在施用该肽后 24 小时和 48 小时诱导印防己毒素引发的惊厥的严重程度增加[5 ].
| Cas No. | 127869-51-6 | SDF | |
| 化学名 | (4R,5E,8Z,10S,11Z,14Z,16S,17Z,19S,20Z,22S,23E,26Z,28S,29Z,31S,32E,34S,35Z,37S,38E,40S,41Z,43S,44Z,47Z,49S,50Z,52R)-52-((Z)-((3Z,5S,6Z,8S,9Z,11S,12Z)-14-amino-5-(4-aminobutyl)-1,4,7,10,13-pentahydroxy-8-(hydroxymethyl)-11-isobutyl-3,6,9,12-tetraazatetradec | ||
| Canonical SMILES | CC[C@]([C@@]1([H])/C(O)=N/C/C(O)=N\[C@@](/C(O)=N/[C@@](/C(O)=N/[C@@](/C(O)=N/C/C(O)=N/[C@@](/C(O)=N/C/C(O)=N\[C@@](C(O)=O)([H])CSSC[C@@](/N=C(O)/C/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/[C@](/N=C(O)/CN)([H])CC(C)C)([H])CO)([H])CCCCN)([H])/C(O)=N/[C@@](/C(O)=N/C | ||
| 分子式 | C93H157N27O28S3 | 分子量 | 2197.61 |
| 溶解度 | H2O : 50 mg/mL (22.75 mM; adjust pH to 3 with 0.5%CH3COOH) | 储存条件 | Desiccate 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 | 0.455 mL | 2.2752 mL | 4.5504 mL |
| 5 mM | 0.091 mL | 0.455 mL | 0.9101 mL |
| 10 mM | 0.0455 mL | 0.2275 mL | 0.455 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。
Once-daily, subcutaneous vosoritide therapy in children with achondroplasia: a randomised, double-blind, phase 3, placebo-controlled, multicentre trial
Lancet2020 Sep 5;396(10252):684-692.PMID: 32891212DOI: 10.1016/S0140-6736(20)31541-5
Background: There are no effective therapies for achondroplasia. An open-label study suggested that vosoritide administration might increase growth velocity in children with achondroplasia. This phase 3 trial was designed to further assess these preliminary findings. Methods: This randomised, double-blind, phase 3, placebo-controlled, multicentre trial compared once-daily subcutaneous administration of vosoritide with placebo in children with achondroplasia. The trial was done in hospitals at 24 sites in seven countries (Australia, Germany, Japan, Spain, Turkey, the USA, and the UK). Eligible patients had a clinical diagnosis of achondroplasia, were ambulatory, had participated for 6 months in a baseline growth study and were aged 5 to less than 18 years at enrolment. Randomisation was done by means of a voice or web-response system, stratified according to sex and Tanner stage. Participants, investigators, and trial sponsor were masked to group assignment. Participants received either vosoritide 15¡¤0 ¦̧/kg or placebo, as allocated, for the duration of the 52-week treatment period administered by daily subcutaneous injections in their homes by trained caregivers. The primary endpoint was change from baseline in mean annualised growth velocity at 52 weeks in treated patients as compared with controls. All randomly assigned patients were included in the efficacy analyses (n=121). All patients who received one dose of vosoritide or placebo (n=121) were included in the safety analyses. The trial is complete and is registered, with EudraCT, number, 2015-003836-11. Findings: All participants were recruited from Dec 12, 2016, to Nov 7, 2018, with 60 assigned to receive vosoritide and 61 to receive placebo. Of 124 patients screened for eligibility, 121 patients were randomly assigned, and 119 patients completed the 52-week trial. The adjusted mean difference in annualised growth velocity between patients in the vosoritide group and placebo group was 1¡¤57 cm/year in favour of vosoritide (95% CI [1¡¤22-1¡¤93]; two-sided p<0¡¤0001). A total of 119 patients had at least one adverse event; vosoritide group, 59 (98%), and placebo group, 60 (98%). None of the serious adverse events were considered to be treatment related and no deaths occurred. Interpretation: Vosoritide is an effective treatment to increase growth in children with achondroplasia. It is not known whether final adult height will be increased, or what the harms of long-term therapy might be. Funding: BioMarin Pharmaceutical.
ASB20123: A novel C-type natriuretic peptide derivative for treatment of growth failure and dwarfism
PLoS One2019 Feb 22;14(2):e0212680.PMID: 30794654DOI: 10.1371/journal.pone.0212680
C-type natriuretic peptide (CNP) and its receptor natriuretic peptide receptor B (NPR-B) are physiological potent positive regulators of endochondral bone growth; therefore, the CNP/NPR-B signaling pathway is one of the most promising therapeutic targets for treating growth failure and dwarfism. In this article, we summarized the pharmacological properties of a novel CNP analog peptide ASB20123 as a therapeutic agent for short stature. ASB20123, one of the CNP/ghrelin chimeric peptides, is composed of CNP(1-22) and human ghrelin(12-28, E17D). Compared to CNP(1-22), ASB20123 showed similar agonist activity for NPR-B and improved biokinetics with a longer plasma half-life in rats. In addition, the distribution of ASB20123 to the cartilage was higher than that of CNP(1-22) after single subcutaneous (sc) injection to mice. These results suggested that the C-terminal part of ghrelin, which has clusters of basic amino acid residues and a BX7B motif, might contribute to the retention of ASB20123 in the extracellular matrix of the growth plate. Multiple sc doses of ASB20123 potently stimulated skeletal growth in rats in a dose-dependent manner, and sc infusion was more effective than bolus injection at the same dose. Our data indicated that high plasma levels of ASB20123 would not necessarily be required for bone growth acceleration. Thus, pharmaceutical formulation approaches for sustained-release dosage forms to allow chronic exposure to ASB20123 might be suitable to ensure drug effectiveness and safety.
C-type natriuretic peptide is associated with the severity of Crimean-Congo hemorrhagic fever
Int J Infect Dis2012 Aug;16(8):e616-20.PMID: 22695238DOI: 10.1016/j.ijid.2012.04.009
Background: Crimean-Congo hemorrhagic fever (CCHF) is characterized by vascular dysfunction, indicating the involvement of endothelial cells. C-type natriuretic peptide (CNP) plays a critical role in the coordination of vascular tone and is associated with the prognosis in critically ill patients such as those with sepsis and septic shock. We investigated whether CNP is related to the severity of CCHF.
Methods: Forty-eight consecutive patients with a laboratory confirmed diagnosis of CCHF and 40 age-sex-matched healthy volunteers as the control group were prospectively enrolled into the study. CCHF patients were classified according to the disease severity into a non-severe group (n=28) and a severe group (n=20).
Results: The CNP levels were detected to be 0.43 (0.4-0.7) ng/ml in the control group, 0.87 (0.7-1.0) ng/ml in the non-severe CCFH group, and 1.27 (0.8-1.7) ng/ml in the severe CCHF group. According to the receiver operating characteristics curve analysis, the optimal cut-off value of CNP to predict disease severity was >1.22 ng/ml, with 89.3% specificity and 55% sensitivity. CNP >1.22 ng/ml, lactate dehydrogenase >480 IU/l, and aspartate aminotransferase >202 IU/l were found to have prognostic significance in the univariate analysis. In the multivariate logistic regression analysis by forward stepwise method, CNP >1.22 ng/ml (odds ratio 8.336, p = 0.016) and lactate dehydrogenase >480 IU/l (odds ratio 16.206, p = 0.002) remained associated with disease severity after adjustment for confounding variables.
Conclusions: CNP measurement could help in the risk stratification of patients with CCHF.
C-type natriuretic peptide neuromodulates via "clearance" receptors
Am J Physiol1995 Apr;268(4 Pt 1):C978-84.PMID: 7733246DOI: 10.1152/ajpcell.1995.268.4.C978
A recently discovered endogenous autacoid, C-type natriuretic peptide, was tested in a pheochromocytoma (PC12) cell line for effects on 1) catecholamine release induced by a depolarizing stimulus, 2) guanylyl and adenylyl cyclase activities, and 3) specific 125I-labeled atrial natriuretic peptide (ANP) binding. C-type natriuretic peptide suppressed evoked neurotransmitter release in the absence of guanylyl cyclase activation or adenylyl cyclase inhibition; however, both a "clearance" (ANP-C) receptor binding agent, des-[Gln18Ser19Gly20Leu21Gly22]-ANF-(4-23)-NH2 (cANF), and pertussis toxin prevented this neuromodulatory effect. The C-type natriuretic peptide preferentially bound to receptors that also bound cANF. The results suggest that C-type natriuretic peptide suppressed evoked neurotransmitter efflux by binding to ANP-C receptors coupled to a pertussis toxin-sensitive process; furthermore, the neuromodulatory effect of C-type natriuretic peptide occurred independently of guanylyl cyclase activation or adenylyl cyclase inhibition. The novel aspects of these findings are 1) neuromodulatory effects of C-type natriuretic peptide, 2) guanylyl cyclase-independent actions of C-type natriuretic peptide, and 3) ANP-C receptors mediating C-type natriuretic peptide actions.
C-type natriuretic peptide and atrial natriuretic peptide receptors of rat brain
Am J Physiol1993 Mar;264(3 Pt 2):R513-23.PMID: 8096124DOI: 10.1152/ajpregu.1993.264.3.R513
Natriuretic peptide receptors in rat brain were mapped by in vitro autoradiography using 125I-labeled [Tyr0]CNP-(1-22) to bind atrial natriuretic peptide receptor (ANPR)-B and ANPR-C receptors selectively, and 125I-labeled alpha-ANP to select ANPR-A and ANPR-C receptors. Des-[Gln18,Ser19,Gly20,Leu21,Gly22]ANP-(4- 23)-amide (C-ANP) was used for its selectivity for ANPR-C over ANPR-A. Specific binding of 125I-[Tyr0]CNP-(1-22) with a dissociation constant (Kd) approximately 1 nM occurred in olfactory bulb, cerebral cortex, lateral septal nucleus, choroid plexus, and arachnoid mater. This binding was abolished by C-type natriuretic peptide [CNP-(1-22)], alpha-ANP and C-ANP, and conformed to ANPR-C. 125I-alpha-ANP bound to all structures that bound 125I-[Tyr0]CNP-(1-22). This binding was also inhibited by both CNP-(1-22) and C-ANP, confirming the presence of ANPR-C-like binding sites. However, ANPR-C-like binding sites were heterogenous because only some had high affinities for 125I-[Tyr0]CNP-(1-22) and CNP-(1-22). 125I-alpha-ANP also bound sites without affinities for C-ANP or CNP-(1-22). These sites were consistent with ANPR-A. They occurred mainly on the olfactory bulb, the choroid plexus, and the subfornical organ. Guanosine 3',5'-cyclic monophosphate production was strongly stimulated by alpha-ANP but not by CNP-(1-22) in olfactory bulb. Neither ligand stimulated it in cortical tissue. Thus the natriuretic peptide binding sites of rat brain conformed to ANPR-A and to heterogenous ANPR-C-like sites. No ANPR-B were detected.