Secretin (human) Hydrochloride

Secretin stimulates the secretion of bicarbonate by the pancreas and inhibits the gastrin and acid production in the stomach. It also potentiates the release of digestive enzymes from the pancreas triggered by cholecystokinin.

Designed for biological research and industrial applications, not intended for individual clinical or medical purposes.

CAT No: 10-101-29

CAS No:108153-74-8 (net)

Synonyms/Alias:RG 1068; RG1068; RG-1068; Secretin

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cGMP Peptide
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M.F/Formula
C130H220N44O40
M.W/Mr.
3037.6
Sequence
H-His-Ser-Asp-Gly-Thr-Phe-Thr-Ser-Glu-Leu-Ser-Arg-Leu-Arg-Glu-Gly-Ala-Arg-Leu-Gln-Arg-Leu-Leu-Gln-Gly-Leu-Val-NH2 hydrochloride salt
Labeling Target
Secretin receptor
Application
Secretin has been widely used in medical field especially in pancreatic functioning test, since it promotes the normal growth and maintenance of the pancreas. Secretin also plays a role in the regulation of body water homeostasis and food intake.
Activity
Ligand
Areas of Interest
Metabolic Disease Neurological Disease
Functions
Secretin receptor activity

Secretin (human) Hydrochloride is a synthetic peptide corresponding to the endogenous human gastrointestinal hormone secretin, presented in its hydrochloride salt form for enhanced stability and solubility. As a linear peptide comprising 27 amino acids, secretin plays a pivotal role in regulating water homeostasis and modulating the secretion of bicarbonate-rich pancreatic fluids in response to acidic chyme entering the duodenum. Its physiological relevance extends to the intricate control of digestive processes, making it an essential tool for researchers studying gut hormone signaling, peptide receptor pharmacology, and the broader landscape of gastrointestinal endocrinology. The availability of Secretin (human) Hydrochloride in research-grade form enables detailed investigation into its biochemical properties, receptor interactions, and downstream signaling pathways.

Peptide receptor studies: Secretin is a prototypical ligand for the secretin receptor, a class B G protein-coupled receptor (GPCR) abundantly expressed in pancreatic and gastrointestinal tissues. Researchers utilize this peptide to characterize receptor binding kinetics, specificity, and downstream activation of intracellular signaling cascades such as cyclic AMP production. Such studies are fundamental for elucidating the molecular mechanisms by which peptide hormones modulate digestive physiology and for evaluating the pharmacological profiles of receptor agonists or antagonists.

Signal transduction research: The availability of human secretin in a pure, synthetic form supports investigations into second messenger systems and signal transduction pathways initiated by peptide hormones. By stimulating target cells or tissues with this peptide, scientists can monitor real-time changes in cAMP levels, protein kinase activation, and gene expression profiles. These experiments provide critical insights into the dynamics of GPCR-mediated signaling and facilitate the dissection of hormone-driven regulatory networks within the gastrointestinal tract and related organs.

Peptide structure-activity relationship (SAR) analysis: Secretin (human) Hydrochloride serves as a reference compound in structure-activity relationship studies aimed at understanding the functional determinants of peptide hormone activity. By comparing the bioactivity of native secretin with that of analogs or modified peptides, researchers can identify key residues responsible for receptor binding and signal transduction efficiency. Such SAR analyses inform the rational design of novel peptide-based probes, agonists, or antagonists for advanced research applications.

Gastrointestinal physiology models: In experimental models of digestive function, secretin is frequently employed to stimulate pancreatic secretion and assess exocrine pancreatic responses under controlled conditions. These applications are instrumental in delineating the physiological roles of peptide hormones in fluid and electrolyte balance, as well as in the development of in vitro and ex vivo systems that mimic human gastrointestinal processes. The use of synthetic secretin ensures reproducibility and specificity in such experimental setups.

Peptide synthesis and assay development: As a well-characterized gastrointestinal peptide, secretin is widely used as a standard or positive control in the development and validation of biochemical assays, such as enzyme-linked immunosorbent assays (ELISAs) and receptor-binding assays. Its defined sequence and biological activity make it an ideal calibrator for quantitative measurements of peptide levels and receptor interactions, supporting robust assay performance in both basic research and high-throughput screening environments.

By providing a reliable and consistent source of Secretin (human) Hydrochloride, researchers are equipped to advance the understanding of peptide hormone biology, dissect receptor-mediated signaling events, and develop innovative tools for gastrointestinal research. Its multifaceted utility across receptor pharmacology, signaling studies, peptide chemistry, and physiological modeling underscores its significance as a foundational reagent in modern biochemical and molecular biology laboratories.

Source#
Synthetic
Solubility
−20°C
Organism
Human
BoilingPoint
N/A
References

Gastric acid secretion is under nervous and hormonal control. Gastrin, the major circulating stimulus of acid secretion, probably does not stimulate the parietal cells directly but acts to mobilize histamine from the ECL cells in the oxyntic mucosa. Histamine stimulates the parietal cells to secrete HCl. The gastrin-ECL cell pathway has been investigated extensively in situ (gastric submucosal microdialysis), in vitro (isolated ECL cells) and in vivo (intact animals). Gastrin acts on CCK2 receptors to control the synthesis of ECL-cell histamine, accelerating the expression of the histamine-forming enzyme histidine decarboxylase (HDC) at both the transcription and the translation/posttranslation levels. Depletion of histamine by alpha-fluoromethylhistidine (an irreversible inhibitor of HDC) prevents gastrin-induced but not histamine-induced gastric acid secretion. Acute CCK2 receptor blockade inhibits gastrin-evoked but not histamine-induced acid secretion. Studies both in vivo/in situ and in vitro have suggested that while acetylcholine seems capable of activating parietal cells, it does not affect histamine secretion from ECL cells. Unlike acetylcholine, the neuropeptides pituitary adenylate cyclase-activating peptide and vasoactive intestinal peptide mobilize ECL-cell histamine. Whether vagally stimulated acid secretion reflects an effect of the enteric nervous system on the ECL cells (neuropeptides) and/or a direct one on the parietal cells needs to be further investigated.

Lindström, E., Chen, D., Norlén, P., Andersson, K., & Håkanson, R. (2001). Control of gastric acid secretion: the gastrin-ECL cell-parietal cell axis. Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology, 128(3), 503-511.

Our understanding of secretin and pancreatic secretions has developed. However, the salient findings of Bayliss and Starling concerning secretin have stood the test of time. Thus secretin is recognized as the key pathway mediating a now classical negative feedback reflex. Acidic chyme, emptying from the stomach, stimulates upper small intestinal mucosal S cells to release secretin. Secretin stimulates the flow of a bicarbonate-rich pancreatic secretion which empties into the duodenum, thus neutralizing the acid chime and removing the stimulus for secretin release. Of wider significance, the concept of hormonal regulation and the definition of a hormone basically remain to this day as originally outlined in Starling's Croonian Lectures.

Hirst, B. H. (2004). Secretin and the exposition of hormonal control. The Journal of physiology, 560(2), 339-339.

Melting Point
N/A

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