Somatostatin
(Synonyms: 生长抑素) 目录号 : GC33669
Somatostatin是一种可抑制生长激素(GH)分泌的十四肽，也可以控制人中枢神经系统中垂体激素的分泌。
Cas No.:51110-01-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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Somatostatin is a tetradecapeptide which can suppress the growth hormone (GH) secretion and control the pituitary hormone secretion in human CNS.
Somatostatin is a tetradecapeptide which can suppress the growth hormone (GH) secretion and control the pituitary hormone secretion in human CNS. Somatostatin has two biologically active forms: the predominant form is the 14 amino-acid long Somatostatin-14 while the more potent form is the amino-terminus extended Somatostatin-28. The biological roles of the two Somatostatin isoforms very strongly overlap and the relative proportions of Somatostatin-14 to Somatostatin-28 vary between different tissues. Somatostatin can reduce adhesion of carcinosarcoma cells to the blood vessels and thus attenuate the metastatic potential of these tumours. Somatostatin can also inhibit monocyte chemotactic migration[1].
[1]. Msaouel P, et al. Somatostatin and somatostatin receptors: implications for neoplastic growth and cancer biology. Expert Opin Investig Drugs. 2009 Sep;18(9):1297-316.
| Cas No. | 51110-01-1 | SDF | |
| 别名 | 生长抑素 | ||
| Canonical SMILES | H-Ala-Gly-Cys-Lys-Asn-Phe-Phe-Trp-Lys-Thr-Phe-Thr-Ser-Cys-OH (Disulfide bridge: Cys3-Cys14) | ||
| 分子式 | 分子量 | 1637.88 | |
| 溶解度 | Water : 50 mg/mL (30.53 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 | 0.6105 mL | 3.0527 mL | 6.1055 mL |
| 5 mM | 0.1221 mL | 0.6105 mL | 1.2211 mL |
| 10 mM | 0.0611 mL | 0.3053 mL | 0.6105 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。
Somatostatin and Somatostatin-Containing Interneurons-From Plasticity to Pathology
Biomolecules 2022 Feb 15;12(2):312.PMID:35204812DOI:10.3390/biom12020312.
Despite the obvious differences in the pathophysiology of distinct neuropsychiatric diseases or neurodegenerative disorders, some of them share some general but pivotal mechanisms, one of which is the disruption of excitation/inhibition balance. Such an imbalance can be generated by changes in the inhibitory system, very often mediated by somatostatin-containing interneurons (SOM-INs). In physiology, this group of inhibitory interneurons, as well as Somatostatin itself, profoundly shapes the brain activity, thus influencing the behavior and plasticity; however, the changes in the number, density and activity of SOM-INs or levels of Somatostatin are found throughout many neuropsychiatric and neurological conditions, both in patients and animal models. Here, we (1) briefly describe the brain somatostatinergic system, characterizing the neuropeptide Somatostatin itself, its receptors and functions, as well the physiology and circuitry of SOM-INs; and (2) summarize the effects of the activity of Somatostatin and SOM-INs in both physiological brain processes and pathological brain conditions, focusing primarily on learning-induced plasticity and encompassing selected neuropsychological and neurodegenerative disorders, respectively. The presented data indicate the somatostatinergic-system-mediated inhibition as a substantial factor in the mechanisms of neuroplasticity, often disrupted in a plethora of brain pathologies.
Somatostatin in neuropsychiatric disorders
Prog Neuropsychopharmacol Biol Psychiatry 1988;12 Suppl:S137-55.PMID:2907936DOI:10.1016/0278-5846(88)90077-2.
1. Somatostatin is a peptide that is widely and discretely distributed throughout the central nervous system. 2. Its relevance to neuropsychiatric disorders is suggested both by the existence of disease-related alterations in Somatostatin content in brain and cerebrospinal fluid as well as by the manifold neuroregulatory capabilities of Somatostatin and related peptides. 3. This article will summarize the central nervous system effects of Somatostatin, identify those neuropsychiatric disorders that are characterized by changes in Somatostatin, and review the evidence for and potential significance of decreases in cerebrospinal fluid Somatostatin in depression.
Somatostatin in portal hypertension
Dig Dis Sci 1989 Mar;34(3 Suppl):40S-47S.PMID:2563965DOI:10.1007/BF01536044.
The effect of Somatostatin on portal pressure is mediated by splanchnic arterial vasoconstriction which induces a reduction in portal blood flow and pressure. One of the most important characteristics of Somatostatin is that its splanchnic effect is not accompanied by major systemic hemodynamic effects. Somatostatin has been used in several controlled trials to test its potential in controlling acute variceal bleeding. The results remain controversial. Different findings in existing clinical trials may derive in part from distinct protocols for Somatostatin administration. Published trials suggest that Somatostatin may be as effective as vasopressin in the acute management of variceal bleeding. However, since the efficacy of vasopressin has been questioned, a comparison of two potentially ineffective drugs cannot establish definitively the efficacy of Somatostatin in controlling variceal bleeding. The most significant finding of the two published studies has been the lower incidence of minor and major complications with Somatostatin when compared to vasopressin. Newer trials in progress may shed new light into the potential use of Somatostatin for the treatment of variceal bleeding.
Overview of Radiolabeled Somatostatin Analogs for Cancer Imaging and Therapy
Molecules 2020 Sep 2;25(17):4012.PMID:32887456DOI:10.3390/molecules25174012.
Identified in 1973, Somatostatin (SST) is a cyclic hormone peptide with a short biological half-life. Somatostatin receptors (SSTRs) are widely expressed in the whole body, with five subtypes described. The interaction between SST and its receptors leads to the internalization of the ligand-receptor complex and triggers different cellular signaling pathways. Interestingly, the expression of SSTRs is significantly enhanced in many solid tumors, especially gastro-entero-pancreatic neuroendocrine tumors (GEP-NET). Thus, Somatostatin analogs (SSAs) have been developed to improve the stability of the endogenous ligand and so extend its half-life. Radiolabeled analogs have been developed with several radioelements such as indium-111, technetium-99 m, and recently gallium-68, fluorine-18, and copper-64, to visualize the distribution of receptor overexpression in tumors. Internal metabolic radiotherapy is also used as a therapeutic strategy (e.g., using yttrium-90, lutetium-177, and actinium-225). With some radiopharmaceuticals now used in clinical practice, Somatostatin analogs developed for imaging and therapy are an example of the concept of personalized medicine with a theranostic approach. Here, we review the development of these analogs, from the well-established and authorized ones to the most recently developed radiotracers, which have better pharmacokinetic properties and demonstrate increased efficacy and safety, as well as the search for new clinical indications.
Somatostatin analogs: does pharmacology impact antitumor efficacy?
Trends Endocrinol Metab 2014 Mar;25(3):115-27.PMID:24405892DOI:10.1016/j.tem.2013.11.003.
Somatostatin is an endogenous inhibitor of secretion and cell proliferation. These features render Somatostatin a logical candidate for the management of neuroendocrine tumors that express Somatostatin receptors. Synthetic Somatostatin analogs (SSAs) have longer half-lives than Somatostatin, but have similar activities, and are used for the treatment of these types of disorders. Interest has focused on novel multireceptor analogs with broader affinity to several of the five Somatostatin receptors, thereby presenting putatively higher antitumor activities. Recent evidence indicates that SSAs cannot be considered mimics of native Somatostatin in regulating signaling pathways downstream of receptors. Here we review this knowledge, discuss the concept of biased agonism, and highlight what considerations need to be taken into account for the optimal clinical use of SSAs.