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Somatostatin-14 (acetate) Sale

目录号 : GC44914

A cyclic peptide hormone

Somatostatin-14 (acetate) Chemical Structure

Cas No.:54472-66-1

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产品描述

Somatostatin-14 is a natural cyclic peptide hormone derived from the preprohormone, somatostatin. It is a somatostatin (SST) receptor agonist that binds to SST1, SST2, SST3, SST4, and SST5 (IC50s = 0.22, 0.10, 0.28, 1.23, and 0.30 nM, respectively, in CCL39 cells expressing human recombinant receptors). It inhibits cAMP accumulation induced by forskolin in CCL39 cells expressing human recombinant SST1, SST2, SST3, SST4, and SST5 (EC50s = 6.16, 4.37, 17.38, 2.95, and 4.67 nM, respectively). Somatostatin-14 inhibits the release of growth hormone, prolactin, thyrotropin, glucagon, and insulin, as well as other signaling molecules.

Chemical Properties

Cas No. 54472-66-1 SDF
Canonical SMILES [H]N[C@H](C(NCC(N[C@H](C(N[C@@H](CCCCN)C(N[C@@H](CC(N)=O)C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@@H](CCCCN)C(N[C@]([C@@H](C)O)([H])C(N[C@H](C(N[C@]([C@@H](C)O)([H])C(N[C@@H](CO)C1=O)=O)=O)CC2=CC=CC=C2)=O)=O)=O)CC3=CNC4=C3C=CC=C4)=O)CC5=CC=CC=C5)=O)CC6=CC=CC
分子式 C76H104N18O19S2•C2H4O2 分子量 1697.9
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1 mg 5 mg 10 mg
1 mM 0.589 mL 2.9448 mL 5.8896 mL
5 mM 0.1178 mL 0.589 mL 1.1779 mL
10 mM 0.0589 mL 0.2945 mL 0.589 mL
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Research Update

Non-endocrine applications of somatostatin and octreotide acetate: facts and flights of fancy

Dis Mon 1991 Dec;37(12):749-848.PMID:1683832DOI:10.1016/s0011-5029(05)80015-x.

Somatostatin, originally detected by Krulich and ultimately isolated by Brazeau, was initially described as a growth hormone release-inhibiting factor. Subsequent investigation into the use of native somatostatin and the development of long-acting somatostatin analogues, especially octreotide acetate, have fostered increasing uses of these compounds. Though the clinical and investigational uses of somatostatin and its analogues are varied, one central theme remains constant: the ability of these agents to suppress circulating peptide levels. This article, a review of the current non-endocrine applications of somatostatin and its analogues, covers a wide range of potential applications for somatostatin-like compounds. These include use in cirrhosis and variceal bleeding, peptic ulcer disease, pancreatic fistulas, acute and chronic pancreatitis, dumping syndrome, cancer therapy, small bowel fistulas, psoriasis, pain control, and autonomic hypotension. Somatostatin may also play a role in the development and potential treatment of neurologic disease and may have profound found influence on behavior.

An update of lanreotide acetate for treatment of adults with carcinoid syndrome

Drugs Today (Barc) 2018 Aug;54(8):457-465.PMID:30209440DOI:10.1358/dot.2018.54.8.2834461.

Carcinoid tumors are rare and usually slow-growing. Some patients with advanced metastatic disease however can develop symptoms of carcinoid syndrome, which results in debilitating diarrhea and flushing. Many treatments including chemotherapy were tried unsuccessfully in the past to treat this syndrome. The symptoms of carcinoid syndrome are thought to be related to the ability of the tumors to produce serotonin. The discovery that the production of this hormone can be inhibited by somatostatin led to the development of somatostatin analogues octreotide and lanreotide, which differ from native somatostatin in that they have a longer half-life. These compounds have shown dramatic responses in symptom control and reduction of serotonin metabolites including urinary 5-hydroxyindoleacetic acid (5-HIAA) levels. This review researches the origins of carcinoid tumors, the development of lanreotide as a treatment and future directions for the treatment of carcinoid syndrome.

Inhibitory effect of Somatostatin-14 on L-type voltage-gated calcium channels in cultured cone photoreceptors requires intracellular calcium

J Neurophysiol 2009 Sep;102(3):1801-10.PMID:19605612DOI:10.1152/jn.00354.2009.

The inhibitory effects of somatostatin have been well documented for many physiological processes. The action of somatostatin is through G-protein-coupled receptor-mediated second-messenger signaling, which in turn affects other downstream targets including ion channels. In the retina, somatostatin is released from a specific class of amacrine cells. Here we report that there was a circadian phase-dependent effect of Somatostatin-14 (SS14) on the L-type voltage-gated calcium channels (L-VGCCs) in cultured chicken cone photoreceptors, and our study reveals that this process is dependent on intracellular calcium stores. Application of 500 nM SS14 for 2 h caused a decrease in L-VGCC currents only during the subjective night but not the subjective day. We then explored the cellular mechanisms underlying the circadian phase-dependent effect of SS14. The inhibitory effect of SS14 on L-VGCCs was mediated through the pertussis-toxin-sensitive G-protein-dependent somatostatin receptor 2 (sst2). Activation of sst2 by SS14 further activated downstream signaling involving phospholipase C and intracellular calcium stores. Mobilization of intracellular Ca2+ was required for somatostatin induced inhibition of photoreceptor L-VGCCs, suggesting that somatostatin plays an important role in the modulation of photoreceptor physiology.

Lanreotide autogel(®): a review of its use in the treatment of patients with acromegaly

Drugs 2014 Sep;74(14):1673-91.PMID:25193626DOI:10.1007/s40265-014-0283-8.

Lanreotide Autogel(®) (ATG) [Somatuline(®) Autogel(®), Somatuline(®) Depot(®)] is a prolonged-release, supersaturated aqueous gel formulation of the somatostatin analogue lanreotide acetate that acts via somatostatin receptors to reduce both growth hormone and insulin-like growth factor-I levels. It is indicated for the treatment of patients with acromegaly who have had an inadequate response to or cannot be treated with surgery and/or radiotherapy. This article reviews the clinical efficacy and tolerability of lanreotide ATG in the treatment of acromegaly, as well as summarizing its pharmacological properties. Results of clinical trials and extension studies of up to 4 years duration showed that deep subcutaneous lanreotide ATG was a generally effective treatment in treatment-naive and treatment-experienced adults with acromegaly. Lanreotide ATG provided hormonal control and improved both health-related quality of life and acromegaly symptoms in most patients; it also reduced tumour volume to a clinically significant extent in studies of primary therapy. Moreover, lanreotide ATG was generally no less effective than intramuscular lanreotide long-acting microparticles and was as effective as intramuscular octreotide long-acting release in switching or crossover studies, including those with standard or extended dosing intervals. Lanreotide ATG is generally well tolerated; the most frequently reported adverse events were mild or moderate transient gastrointestinal symptoms. Lanreotide ATG also has the advantage of being available in a convenient pre-filled syringe and is given subcutaneously rather than intramuscularly. Thus, lanreotide ATG continues to be a valuable option in the treatment of acromegaly, with potential advantages being ease of administration and longer dosing intervals in patients who have an adequate response to initial therapy.

Somatostatin binding reduced by ammonium acetate in the rat hippocampus can be reversed by treatment with N-carbamyl-L-glutamate plus L-arginine

Synapse 1992 Sep;12(1):55-61.PMID:1357763DOI:10.1002/syn.890120107.

The effects of short-term (90 min), mid-term (5 days), and long-term (15 days) administration of ammonium acetate (5 mmol/Kg day i.p.) on the somatostatinergic neurotransmitter system of the rat hippocampus have been studied. Scatchard analysis of the binding of 125I-Tyr11-somatostatin to hippocampal dissociated cells indicated that administration of ammonium acetate at the times studied were associated with a decrease in the number of somatostatin receptors in this brain area, whereas the affinity of the same receptors remained unchanged. Administration of ammonium acetate did not affect the levels of somatostatin-like immunoreactivity in the hippocampus. Treatment with N-carbamyl-L-glutamate (1 mmol/Kg, i.p.) plus L-arginine (1 mmol/kg), which lead to the conversion of ammonia into urea, prevented the ammonium acetate-induced changes in somatostatin binding in this brain area. N-carbamyl-L-glutamate plus L-arginine alone had no observable effect on the somatostatinergic system. The decrease in the number of somatostatin receptors induced by ammonium acetate might reflect a decreased sensitivity of the target cells to somatostatin, a phenomenon that could contribute to the depressed neuronal excitability induced by ammonia in the rat hippocampus.