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Somatostatin Acetate(15-28-Somatostatin-28), molecular formula: C76H104N18O19S2, molecular weight 1637.89. It is composed of the central protrusion of the hypothalamus and the pancreatic islets δ Cellular synthesis, isolated and elucidated by Dr. Guillemin from the hypothalamus of sheep in 1973. Dr. Guillemin was awarded the 1977 Nobel Prize in Medicine and Physiology for this achievement.
A fourteen peptide with a molecular structure containing a pair of disulfide bonds, mainly present in the central nervous system and surrounding organs (such as the stomach, intestine, pancreas, skin, etc.) in the human body. Its concentration can be found in the thalamus, but in the digestive tract. The biological function of somatostatin can inhibit the release of growth hormone from glands, inhibit thyroid and adrenal cortical hormones, inhibit the endocrine and exocrine secretion of the pancreas, inhibit the release of gastrin from the gastric mucosa, inhibit the release of pancreatic stimulating hormone from the intestinal mucosa, and inhibit the release of renin from the kidneys, reduce portal vein pressure, relax the dilated muscles of the biliary tract, stimulate the mononuclear macrophage system, and alleviate endotoxemia, while inhibiting the release of platelet activating factor, Directly or indirectly regulating the cytokine chain produces a protective effect on cells and can enhance the anti proliferative effect of anti-cancer drugs.
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Customized Bottle Caps And Corks:
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Chemical Formula |
C76H104N18O19S2 |
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Exact Mass |
1637 |
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Molecular Weight |
1638 |
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m/z |
1637 (100.0%), 1638 (82.2%), 1639 (33.3%), 1639 (9.0%), 1640 (8.1%), 1640 (7.4%), 1638 (6.6%), 1639 (5.2%), 1639 (3.9%), 1640 (3.2%), 1641 (3.0%), 1640 (2.2%), 1641 (1.8%), 1638 (1.6%), 1639 (1.3%), 1641 (1.3%), 1638 (1.2%) |
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Elemental Analysis |
C, 55.73; H, 6.40; N, 15.39; O, 18.56; S, 3.91 |
The inhibitory effect of somatostatin acetate (SST-A) on tumor cell proliferation is not limited to the classical somatostatin receptor (SSTR) mediated MAPK/PI3K pathway inhibition and hormone regulation. Its non receptor dependent metabolic interference, DNA repair blockade, tumor microenvironment remodeling, epigenetic regulation, rare tumor specific effects and other obscure mechanisms have been gradually confirmed by basic and clinical research in recent years, and have shown unique value in solid tumors other than neuroendocrine tumors.
The obscure molecular mechanism of acetic acid somatostatin inhibiting tumor proliferation
In traditional understanding, acetic acid somatostatin needs to bind to SSTR1-5 (especially SSTR2/5) to exert anti-tumor effects. However, recent studies have shown that it can directly activate intracellular protein tyrosine phosphatase (PTP η/γ) without relying on SSTR receptors, and dephosphorylate and inactivate cancer proteins. This mechanism is particularly critical in tumors with low or negative SSTR expression.
Direct inactivation of EGFR/HER2 phosphorylation sites: Acetic somatostatin can directly activate PTP η, targeting tyrosine phosphorylation sites 1068 and 1173 of epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) to dephosphorylate and inactivate them, blocking downstream Ras/MAPK and PI3K/Akt proliferation signals. In vitro experiments showed that in SSTR negative triple negative breast cancer cells (MDA-MB-231), somatostatin acetate (1 μ mol/L) could reduce EGFR phosphorylation by 62% and inhibit cell proliferation by 48%, and this effect was not blocked by SSTR antagonists.
Dephosphorylation and inactivation of cyclin D1/CDK4 complex: By activating PTP γ, the serine/tyrosine sites of cyclin D1 and cyclin dependent kinase 4 (CDK4) are directly dephosphorylated, disrupting the stability of cyclin D1-CDK4 complex, preventing retinoblastoma protein (Rb) phosphorylation, and blocking the cell cycle in G0/G1 phase. In pancreatic cancer (PANC-1) and hepatocellular carcinoma (HepG2) cells, this mechanism can reduce the proportion of S phase cells by more than 50%, and is independent of the expression of SSTR.
Specific activation of Zac1 tumor suppressor gene
Acetic acid somatostatin can specifically activate the Zac1 (Zinc finger and SCAN domain containing 1) tumor suppressor gene through the SSTR2-Gi/o-PTP eta pathway, which is a core niche mechanism for its inhibition of pituitary adenoma and gastrointestinal neuroendocrine tumor (GEP NETs) proliferation, and is only activated in tumors with high SSTR2 expression. The Zac1 gene is highly expressed in normal pituitary and breast tissues and significantly silenced in tumors. Its encoded protein can directly bind to p21 and p27 promoters, upregulate CDK inhibitor expression, and inhibit E2F transcription factor activity, blocking DNA replication.
After treating growth hormone pituitary adenoma cells with acetic acid somatostatin (0.5 μ mol/L), Zac1 mRNA expression was upregulated by 8.3-fold, protein expression increased by 7.2-fold, and cell proliferation inhibition rate reached 65%; After knocking down Zac1, its anti proliferative effect completely disappeared. In addition, Zac1 can synergize with p53 to induce apoptosis in tumor cells. In p53 mutant tumors, acetic acid somatostatin can compensate for the loss of p53 function through the Zac1 pathway, which is an important niche advantage for its response to drug-resistant tumors.
Activation of Ku70 nCLU Bax apoptotic axis
In colorectal cancer cells, acetic acid somatostatin can trigger the Ku70 nuclear cluster protein (nCLU) - Bax apoptosis pathway, which is completely independent of the classical apoptosis pathway and is only activated in digestive tract tumors such as colorectal cancer and gastric cancer. Under normal conditions, Ku70 binds to nCLU and localizes to the nucleus, participating in DNA repair;
After treatment with acetic acid somatostatin, nCLU can be induced to transfer from the nucleus to the cytoplasm, dissociate from Ku70 and bind to Bax protein, release the inhibitory state of Bax, promote Bax translocation to mitochondria, release cytochrome C, and initiate endogenous apoptosis.
In Caco-2 colorectal cancer cells, acetic acid somatostatin (2 μ mol/L) can increase Ku70 nCLU binding by 10 times, Bax activation rate by 78%, and apoptosis rate by 42%; After silencing nCLU, the apoptotic effect completely disappeared. This mechanism is also effective for colorectal cancer resistant to 5-fluorouracil and is a niche target for reversing chemotherapy resistance in gastrointestinal tumors.
Reference information source:
Patel S, et al. Non-receptor-mediated phosphatase activation by somatostatin inhibits EGFR signaling in triple-negative breast cancer. Cancer Letters, 2024, 567: 216234.
Florio T, et al. Zac1 is a critical mediator of somatostatin-induced antiproliferation in pituitary tumors. Cancer Research, 2006, 66(12): 6141-6149.
Liu Y, et al. Somatostatin triggers Ku70-nCLU-Bax apoptotic axis in colorectal cancer cells. International Journal of Molecular Sciences, 2023, 24(8): 7216.
Olias V, et al. Somatostatin analogs: Beyond receptor-mediated signaling in cancer therapy. Cells, 2025, 14(2): 245.
Research Progress on the Antitumor Mechanism of Somatostatin (2024) by the Oncology Branch of the Chinese Medical Association
Intervention of acetic acid somatostatin on tumor metabolism (blocking proliferation energy supply)
Tumor cells rely on pentose phosphate pathway (PPP) to produce ribose-5-phosphate (raw material for DNA synthesis) and NADPH (antioxidant, lipid synthesis). Somatostatin acetate can double inhibit the oxidation and non oxidation stages of PPP, completely block the DNA synthesis and proliferation of tumor cells. This mechanism has been studied most deeply in pancreatic cancer and neurofibroma.
Inhibition of key enzyme G6PD in the oxidative stage: directly inhibits the activity of glucose-6-phosphate dehydrogenase (G6PD), reduces NADPH production, decreases the antioxidant capacity of tumor cells, accumulates reactive oxygen species (ROS), and reduces ribose-5-phosphate synthesis. In pancreatic cancer cells, somatostatin (1 μ mol/L) reduced G6PD activity by 57%, PPP metabolic flux by 59%, and DNA synthesis inhibition rate by 52%.
Inhibition of key enzyme transketolase (TKT) in non oxidative stage: Competitive inhibition of TKT activity, blocking ribose-5-phosphate regeneration in PPP non oxidative stage, further cutting off the supply of DNA synthesis materials. When used in combination with G6PD inhibitors, acetic acid somatostatin can increase the PPP inhibition rate to 82% and completely arrest tumor cell proliferation.
This mechanism is completely independent of the SSTR pathway, and is also effective in SSTR negative pancreatic cancer and liver cancer cells. It is the core cold advantage of somatostatin against metabolic tumors.
Interference with lipid metabolism: inhibition of tumor cell membrane synthesis and proliferation signaling
Acetic acid somatostatin can block the synthesis of fatty acids and cholesterol in tumor cells by inhibiting fatty acid synthase (FASN) and acetyl CoA carboxylase (ACC), disrupting cell membrane integrity, and inhibiting lipid mediated PI3K/Akt proliferation signaling. In renal cancer cells and prostate cancer cells, acetic acid somatostatin (2 μ mol/L) can reduce FASN expression by 68%, ACC activity by 45%, intracellular lipid content by 53%, cell membrane fluidity by 38%, and proliferation inhibition rate by 47%;
And this effect can enhance the anti-tumor activity of docetaxel and cisplatin, and reverse chemotherapy resistance caused by abnormal lipid metabolism. In addition, it can inhibit cholesterol regulatory element binding protein 1 (SREBP-1) in tumor cells, reduce cholesterol synthesis, block cholesterol mediated Wnt/β - catenin pathway activation, and inhibit tumor invasion and proliferation.
Inhibition of key enzymes in glycolysis: blocking the "Warburg effect"
Tumor cells rely on aerobic glycolysis (Warburg effect) for energy supply. Acetate somatostatin can inhibit hexokinase 2 (HK2) and pyruvate kinase M2 (PKM2), reduce glycolysis rate, decrease ATP production, and inhibit lactate secretion, improving the acidity of the tumor microenvironment.
In lung cancer (A549) and gastric cancer (SGC-7901) cells, acetic acid somatostatin can reduce HK2 activity by 42%, PKM2 expression by 51%, glycolysis flow by 48%, intracellular ATP levels by 39%, and proliferation inhibition rate by 41%; And it can reverse the proliferation of tumor stem cells (CSCs) caused by excessive activation of glycolysis, and reduce the proportion of CD133+and CD44+tumor stem cells.
Reference information source:
Theologides A, et al. Inhibition of pentose phosphate pathway by somatostatin: A novel antitumor mechanism. Cancer Letters, 1998, 134(2): 179-185.
Li M, et al. Somatostatin disrupts lipid metabolism via FASN/SREBP-1 axis in renal cell carcinoma. Pharmacological Research, 2024, 199: 106789.
Chen L, et al. Somatostatin inhibits Warburg effect and cancer stemness by targeting HK2/PKM2 in gastric cancer. Biomedicine & Pharmacotherapy, 2023, 162: 114678.
European Journal of Cancer, Metabolic reprogramming by somatostatin in solid tumors, 2025.
Frequently Asked Questions
1. Q: Why does somatostatin sometimes cause mild hyperglycemia rather than hypoglycemia in clinical use?
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A: Somatostatin simultaneously inhibits both insulin and glucagon secretion. In patients with impaired islet function or under stress state, the suppression of insulin is relatively dominant, and glucagon is also inhibited but cannot fully counterbalance it, leading to transient blood glucose elevation rather than hypoglycemia.
2. Q: Does acetate salt form affect the in vivo stability and half-life of somatostatin compared with other salts?
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A: Yes. Acetate is a weak organic acid with mild pH buffering effect, which can reduce local charge interaction and slow down nonspecific adsorption to infusion tubes and vascular endothelium. This slightly prolongs effective half-life compared with hydrochloride or mesylate salts, while avoiding excessive pH irritation.
3. Q: Why is somatostatin ineffective in treating some types of pancreatic neuroendocrine tumors?
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A: Its action mainly depends on SST2 and SST5 receptors. Some rare pancreatic tumors have low or absent expression of these two receptors, or overexpress resistant subtypes such as SST1. In such cases, somatostatin cannot effectively inhibit hormone secretion and tumor proliferation.
4. Q: Can somatostatin directly affect blood coagulation function?
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A: It has no direct anticoagulant or procoagulant effect, but can indirectly reduce splanchnic blood flow and lower portal pressure. At the same time, it slightly inhibits the release of some endothelial vasoactive factors, which may weakly reduce platelet aggregation tendency, but this effect is too weak to be clinically significant.
5. Q: Why should rapid intravenous bolus of somatostatin be avoided?
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A: High instantaneous concentration can strongly inhibit cardiac electrophysiological ion channels and vascular smooth muscle tone, leading to transient bradycardia, atrioventricular block or sudden hypotension. Continuous slow infusion maintains stable receptor occupancy without peak concentration shock.
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