Product Information

Registration Status: Active

STILAMIN 3000 FOR INJECTION 3mg/AMPOULE is approved to be sold in Singapore with effective from 1991-06-17. It is marketed by MERCK PTE LTD, with the registration number of SIN06135P.

This product contains Somatostatin 3mg/ampoule in the form of INJECTION, POWDER, FOR SOLUTION. It is approved for INTRAVENOUS use.

This product is manufactured by Merck Serono S.A. in SWITZERLAND.

It is a Prescription Only Medicine that can only be obtained from a doctor or a dentist, or a pharmacist with a prescription from a Singapore-registered doctor or dentist.



Somatostatin, also known as growth hormone-inhibiting hormone, is a naturally-occurring peptide hormone of 14 or 28 amino acid residues [T28] that regulates the endocrine system. It is secreted by the D cells of the islets to inhibit the release of insulin and glucagon, and is also generated in the hypothalamus, where it inhibits the release of growth hormone and thyroid-stimulating hormones from the anterior pituitary [T28]. Somatostatin is initially secreted as a 116 amino acid precursor, preprosomatostatin, which undergoes endoproteolytic cleavage to prosomastatin. Prosomastatin is further process into two active forms, somatostatin-14 (SST-14) and somatostatin-28 (SST-28), an extended SST-14 sequence to the N-terminus [A20384]. The actions of somatostatin are mediated via signalling pathways of G protein-coupled somatostatin receptors. Antineoplastic effects and potential uses of somatostatin on various tumours, including pituitary adenomas, GEP-NETs, paragangliomas, carcinoids, breast cancers, malignant lymphoma and small-cell lung cancers, have been extensively investigated [A20384]. Somatostatin has been used in the clinical setting for the diagnosis of acromegaly and gastrointestinal tract tumours. Its analogues have been developed to achieve more favourable kinetics for efficiency use in the management of acute conditions, such as esophageal varices. [DB00104] is a long-acting analogue of somatostatin that inhibits the release of a number of hormones, and is clinically used to relieve symptoms of uncommon gastroenteropancreatic endocrine tumours, as well as treat acromegaly [T28].


For the symptomatic treatment of acute bleeding from esophageal varices. Other treatment options for long-term management of the condition may be considered if necessary, once initial control has been established.

Mechanism of Action

Somatostatin binds to 5 subtypes of somatostatin receptors (SSTRs), which are all Gi-protein-coupled transmembrane receptors that inhibits adenylyl cyclase upon activation [A20384]. By inhibiting intracellular cyclic AMP and Ca2+ and by a receptor-linked distal effect on exocytosis, SSTRs block cell secretion [A27323]. The common pathway shared by the receptors involve the activation of phosphotyrosine phosphatase (PTP), and modulation of mitogen-activated protein kinase (MAPK) [A27323]. With the exception of SSTR3, activation of SSTRs lead to activation of voltage-gated potassium channels accompanied by increased K+ currents. This result in membrane hyperpolarization and inhibits depolarization-induced Ca2+ influx through voltage-sensitive Ca2+ channels [A20384]. Depending on the receptor subtype, signalling cascades involve activation of other downstream targets such as Na+/H+ exchanger, Rho GTPase, and nitric oxide synthase (NOS) [A20384]. SSTRs 1 to 4 bind both somatostatin isoforms with equal nanomolar binding affinity whereas SSTR5 exhibits a 5- to 10-fold higher binding affinity for SST-28 [A20384]. **Effects of SSTR1:** Upon biding of somatostatin and activation, SSTR1 mediates an antisecretory effect on growth hormone, prolactin and calcitonin [A20384]. **Effects of SSTR2:** SSTR2 subtype dominates in endocrine tissues. By binding to SST2 receptors, somatostatin exerts paracrine inhibitory actions on gastrin release from G cells, histamine release from ECL cells, and directly on parietal cell acid output [T28]. SSTR2 receptor signalling cascades also inhibit the secretion of growth hormone and that of adrenocorticotropin, glucagon, insulin, and interferon-γ [A20384]. **Effects of SSTR3:** Activation of these receptors lead to reduction in cell proliferation [A20384]. SSTR3 triggers PTP-dependent cell apoptosis accompanied by activation of p53 and the pro-apoptotic protein Bax [A27323]. A study of the matrigel sponge assay suggests that through SSTR3-mediated inhibition of both NOS and MAPK activities may lead to the antitumor effects of somatostatin in inhibiting tumor angiogenesis [A32606]. **Effects of SSTR4:** The functions of SSTR4 remain largely unknown [A20384]. **Effects of SSTR5:** Like SSTR2, SSTR5 subtype also predominates in endocrine tissues. Upon activation, SSTR5 signalling cascades exert an inhibitory action on growth hormone, adrenocorticotropin, insulin, and glucagon-like peptide-1 as well as the secretion of amylase [A20384]. The presence of somatostatin receptors has been identified in most neuroendocrine tumours, endocrine gastroenteropancreatic (GEP) tumors, paragangliomas, pheochromocytomas, medullary thyroid carcinomas (MTC) and small cell lung carcinomas [A32600]. The antitumor effects of somatostatin were also effective in various malignant lymphomas and breast tumours [A32600]. Gastrointestinal hormones, such as gastrin, secretin, and cholecystokinin (CCK), as well as growth hormones and growth factors are thought to be elevated in gastrointestinal tract and neuroendocrine tumours and are inhibited by somatostatin [A32595]. _In vitro_, somatostatin inhibited epidermal growth factor (EGF)-induced DNA synthesis and replication following which suggest that somatostatin may have direct anti-proliferative effects via SSTR signalling [A32595]. Acromegaly is characterized as the endocrine disorder caused by a functioning tumour of cells that secrete growth hormone from the anterior pituitary [T28]. Somatostatin analogue therapies serve to normalize the elevated levels of GH and insulin-like growth factor 1 (IGF-1) and attenuate tumour growth. In the vascular system this likely produces vasoconstriction by inhibiting adenylate cyclase leading to a lowering the concentration of cyclic adenosine monophosphate in the endothelial cells which ultimately blocks vasodilation through this pathway. This vasoconstriction is though the be responsible for reducing blood flow to the esophageal tissues and so reduces bleeding from esophageal varices [A27145]. Somatostatin mediates an analgesic activity by reducing vascular and nociceptive components of inflammation [A32599]. Studies indicate that somatostatin may be present in nociceptive DRG neurons with C-fibers and primary afferent neurons to inhibit the release of transmitters at the presynaptic junctions of the sensory-efferent nerve terminals [A20384]. Exogenous somatostatin has shown to inhibit the release of Substance P from central and peripheral nerve ending [A20384].


This pharmacokinetic data is irrelevant.
This pharmacokinetic data is irrelevant.
Somatostatin is rapidly degraded by peptidase enzymes present in cells and plasma [A20384].


Following intravenous administration of 3H-labeld endogenous somatostatin, the total body clearance was approximately 50 mL/min [A32596]. In man, the value was calculated to be as high as 3000 mL/minutes, which is greatly exceeds the hepatic blood flow. This suggests that rapid enzymatic breakdown in the circulation and other tissues serves as a critical route of elimination [A32596].


Data is not available.

Active Ingredient/Synonyms

Somatostatina | Somatostatine | Somatostatinum | Synthetic growth hormone release-inhibiting hormone | Synthetic somatostatin-14 | Somatostatin |

Source of information: Drugbank (External Link). Last updated on: 3rd July 18. *Trade Name used in the content below may not be the same as the HSA-registered product.


  1. Health Science Authority of Singapore - Reclassified POM
  2. Drugbank