SSTR2/3/5
Akt/GSK3β signaling pathway - Octreotide improves hepatic glycogen synthesis by increasing the phosphorylation of Akt (Ser473) and GSK3β (Ser9), which leads to activation of glycogen synthase (GS) [1]
.
- Glycogen synthase (GS) - Octreotide increases GS mRNA expression levels, promoting hepatic glycogen synthesis [1]
.
- Insulin resistance - Octreotide improves insulin sensitivity as evidenced by reduced HOMA index values [1]
.

In HepG2 cells, octreotide reverses PA-induced Akt and GSK3β phosphorylation as well as alterations in the expression of GS mRNA [1]. Increased glycogen and phosphorylated glycogen synthase switching 3β (GSK3β) are the results of octreotide (10 8mM, 6 hours).

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Cell Model: Human hepatoblastoma HepG2 cells were used to establish an in vitro fatty liver model. Cells were treated with palmitate (PA, 125 μM) plus 0.5% BSA for 24 hours to induce lipid accumulation and insulin resistance. Octreotide (10⁻⁸ mmol/L) was added for 6 hours, followed by insulin (100 μM) stimulation for 20 minutes before cell collection [1]
.
- Lipid Accumulation: Oil Red O staining showed that octreotide treatment significantly alleviated PA-induced lipid droplet accumulation in HepG2 cells. IOD values were significantly lower in the octreotide-treated group compared to PA-only group (P<0.01) [1]
.
- Akt/GSK3β Signaling: Western blot analysis showed that PA treatment significantly reduced the phosphorylation of Akt (by 74.2%) and GSK3β (by 18.7%) compared to control. Octreotide treatment significantly reversed these reductions, increasing p-Akt by 140.8% and p-GSK3β by 12.2% compared to PA group (P<0.05) [1]
.
- Glycogen Synthase mRNA: RT-qPCR analysis showed that PA treatment significantly reduced GS mRNA levels. Octreotide treatment significantly increased GS mRNA expression compared to PA group (0.940±0.07 vs. 0.60±0.08, P<0.05) [1]
.

In the HFD dynamic group, octreotide dramatically lowered insulin concentrations. Octreotide was found to dramatically lower insulin concentrations, but not serum TG, TC, FFA, ALT, or AST levels. The HOMA index is severely inhibited by octreotide. The AUC of ipGTT and ipITT was somewhat reduced by octreotide. In PA-treated HepG2, octreotide reduces steatosis of fat storage caused by HFD cells and lipid droplet accumulation. In HFD fat storage, octreotide stimulates the phosphorylation of Akt and GSK3β as well as the expression of GS mRNA [1]. It also decreased body weight and wet kidney weight in comparison to the crown substance therapy (CONT) group. Treatment with PAS and octreotide/PAS decreased cAMP levels, but octreotide by itself did not lower PCK. The number of pS6-positive cells was considerably lower in the octreotide/PAS group than in the PAS alone group [2].

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Animal Model: Male Sprague-Dawley rats (3 weeks old, 40-60 g) were fed a high-fat diet (HFD, 500 kcal/100 g, 60% calories from fat) for 24 weeks to induce obesity. Rats with body weight ≥1.4-fold higher than controls were selected. Obese rats were divided into HFD-control group (n=12) and octreotide-treated group (n=12). Octreotide was administered by subcutaneous injection at 40 μg/kg body weight every 12 hours for 8 days while continuing HFD feeding [1]
.
- Body Weight and Obesity Parameters: Octreotide treatment significantly reduced body weight (606.58±57.11 g in HFD group vs. 534.42±49.15 g in octreotide group, P<0.01), liver weight (14.88±1.41 g vs. 12.46±1.05 g, P<0.01), abdominal fat (28.87±8.76 g vs. 20.02±4.83 g, P<0.01), and abdominal fat index (4.72±1.23% vs. 3.75±0.81%, P<0.05). Lee's index showed a non-significant decrease [1]
.
- Blood Glucose and Insulin: Octreotide significantly reduced fasting plasma glucose (6.26±1.55 mmol/L in HFD group vs. 4.75±1.60 mmol/L in octreotide group, P<0.01) and serum insulin levels (157.68±43.55 mmol/L vs. 108.85±66.36 mmol/L, P<0.05) [1]
.
- Insulin Sensitivity: The HOMA index, a measure of insulin resistance, was significantly reduced by octreotide treatment (39.57±13.48 in HFD group vs. 23.40±16.71 in octreotide group, P<0.01), indicating improved insulin sensitivity [1]
.
- Glucose and Insulin Tolerance Tests: ipGTT and ipITT showed that octreotide treatment decreased the area under the curve (AUC) by 5.2% and 10.5% respectively compared to HFD group, though these changes did not reach statistical significance [1]
.
- Serum Lipids and Liver Enzymes: Octreotide treatment decreased serum TG, TC, FFA, ALT, and AST levels compared to HFD group, but these changes were not statistically significant [1]
.
- Hepatic Lipid Content: Octreotide significantly reduced hepatic triglyceride (TG) levels (29.94±14.63 mg/g liver in HFD group vs. 18.11±7.08 mg/g liver in octreotide group, P<0.01) and hepatic free fatty acid (FFA) levels (61.22±16.04 mmol/g protein vs. 40.86±5.09 mmol/g protein, P<0.01) [1]
.
- Hepatic Glycogen Content: Octreotide significantly increased hepatic glycogen content (3.66±0.84 mg/g protein in HFD group vs. 4.77±0.78 mg/g protein in octreotide group, P<0.05) [1]
.
- Hepatic Steatosis: H&E staining and Oil Red O staining of liver tissues showed that octreotide treatment significantly improved HFD-induced hepatic steatosis, reducing fat deposition and lipid infiltration. Integrated optical density (IOD) values for Oil Red O staining were significantly lower in the octreotide group compared to HFD group (P<0.01) [1]
.
- Akt/GSK3β Signaling in Liver: Western blot analysis showed that octreotide treatment significantly increased the phosphorylation of Akt (Ser473) and GSK3β (Ser9) in liver tissues compared to HFD group (P<0.05). GS mRNA levels were also significantly increased by octreotide treatment (P<0.05) [1]
.

cAMP Radioimmunoassay: Renal tissue cAMP content was measured using a cAMP radioimmunoassay kit. Kidneys were homogenized with HCl, and extracted cAMP levels were analyzed and corrected by protein concentration [2]
.

Western Blot analysis [3]
Cell Types: Human hepatoblastoma HepG2 cell line
Tested Concentrations: 10-8mM
Incubation Duration: 6 hrs (hours)
Experimental Results: The protein expression levels of phospho-Akt and GSK3β increased by 140.8%. and 12.2%, the mRNA levels of GS were also increased.

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Cell Culture: HepG2 cells were cultured in RPMI-1640 medium with 10% FBS, 100 U/mL penicillin, and 100 μg/mL streptomycin at 37°C with 5% CO₂. At 80% confluence, cells were starved overnight in serum-free or low-serum (0.5% FBS) medium [1]
.
- Experimental Groups: Control group (0.5% BSA for 24 h), PA-treated group (125 μM PA + 0.5% BSA for 24 h), and PA + octreotide group (125 μM PA + 0.5% BSA for 24 h, then 10⁻⁸ mmol/L octreotide for 6 h). All groups received 100 μM insulin for 20 min before collection [1]
.
- Oil Red O Staining: Cells were washed with PBS, fixed with 4% formaldehyde for 30 min, washed with 60% isopropyl alcohol, stained with 0.3% Oil Red O working solution for 30 min at 37°C, and counterstained with 0.2% hematoxylin. Images were captured and IOD values analyzed [1]
.
- RT-qPCR: Total RNA was extracted using TRIzol reagent. RNA (2 μg) was reverse transcribed to cDNA. qPCR was performed using SYBR-Green Master Mix with specific primers for GS and β-actin. Relative expression was calculated using the 2⁻ΔΔCq method [1]
.
- Western Blotting: Total protein was isolated using a whole cell assay kit. Protein concentrations were measured by BCA assay. Proteins (40 μg) were separated by 10% SDS-PAGE, transferred to PVDF membranes, blocked with 5% non-fat milk, and incubated with primary antibodies against p-Akt (Ser473), p-GSK3β (Ser9), Akt, GSK3β, and β-actin overnight at 4°C, followed by HRP-conjugated secondary antibodies. Bands were detected using ECL reagent and analyzed with Quantity One software [1]
.

A total of 24 eligible rats were separated from the HFD group at random and divided into the HFD-control group (n=12) and the octreotide (OCT)-treated group (n=12). These groups were continuously fed a HFD for 8 days, and rats in the octreotide-treated group were subcutaneously injected with octreotide at a dose of 40 µg/kg body weight every 12 h for 8 days. During the octreotide administration period, body weight and food intake were monitored daily. At the end of the experiment, all rats underwent a 12-h starvation period and were sacrificed with 2% sodium pentobarbital (45 mg/kg body weight) administered intraperitoneally. Following sacrifice, blood samples were collected and centrifuged at 860 × g for 15 min at 4°C, and the supernatant was stored at −80°C for further analysis. The liver tissues were isolated, and one sample was rapidly frozen in liquid nitrogen prior to storage at −80°C for total RNA and protein extraction or Oil Red O staining. A second sample was fixed in 4% paraformaldehyde for 48 h at room temperature for histological examination. Abdominal fat was also collected and weighed.[1]

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Male PCK rats (n = 24) were assigned randomly to 1 of 4 groups (n = 6 per group): treatment by subcutaneous injection every 4 weeks treatment with 8 mg/kg octreotide (OCT)-LAR alone, 8 mg/kg PAS-LAR alone, co-application of 8 mg/kg OCT and 8 mg/kg PAS, or vehicle (microparticles liquid; CONT) from 4 to 16 weeks of age. The vehicle contains copolymer microparticles with polylactic-co-glycolic acid (PLGA), obtained from Novartis. In 4- and 15-week-old conscious rats, heart rate (HR), diastolic blood pressure (DBP), and systolic blood pressure (SBP) were determined using a tail-cuff sphygmomanometer. Twenty-four-hour urine volume and food consumption were measured using metabolic cages after 15.5 weeks of age. After body weight measurement, the animals were anesthetized with sodium pentobarbital at 16 weeks of age, and the kidneys and liver were removed rapidly, causing lethal exsanguination. Total wet kidney weight and wet liver weight were measured, and blood samples were collected for measurements of serum urea nitrogen (SUN), aspartate amino transferase (AST), alanine aminotransferase (ALT), insulin-like growth factor-1 (IGF-1), glucose, insulin, glucagon, and cortisol.[2]

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Animals and Diet:** Male Sprague-Dawley rats (3 weeks old, 40-60 g) were housed under standard conditions. After 7 days acclimation on standard diet, rats were divided into normal diet group (320 kcal/100 g, 4.65% fat, n=12) and HFD group (500 kcal/100 g, 60% fat, n=28) for 24 weeks [1]
.
- **Drug Administration:** Octreotide was administered subcutaneously at 40 μg/kg body weight every 12 hours for 8 days to obese rats (body weight ≥1.4-fold higher than controls). HFD-control group received no treatment [1]
.
- **Monitoring:** Body weight, body length, and tail length were measured weekly. Food intake was monitored daily during octreotide administration [1]
.
- **Glucose and Insulin Tolerance Tests:** After 12 h fasting, rats received intraperitoneal glucose (2.0 g/kg) or insulin (7.5 U/kg). Blood samples were collected from tail vein at 0, 15, 30, 60, and 120 min post-injection. Glucose levels were measured using a glucometer. AUC was calculated using GraphPad Prism [1]
.
- **Sample Collection:** At the end of experiment, rats were fasted for 12 h and sacrificed with 2% sodium pentobarbital (45 mg/kg, i.p.). Blood samples were collected, centrifuged at 860×g for 15 min at 4°C, and serum stored at -80°C. Liver tissues were isolated for histological analysis, RNA/protein extraction, or frozen for Oil Red O staining [1]
.
- **Lee's Index Calculation:** Lee's index = [Body weight (g)¹ᐟ³ × 1000] / body length (cm) [1]
.
- **HOMA Index Calculation:** HOMA index = [FPG (mmol/L) × fasting serum insulin (μU/mL)] / 22.5 [1]
.
- **Liver Histology:** Paraffin-embedded liver sections were stained with H&E for morphological evaluation. Frozen liver sections were stained with Oil Red O for lipid assessment. IOD values were analyzed using Image Pro Plus software [1]
.
- **Hepatic TG Measurement:** Liver tissue (50 mg) was homogenized in chloroform-methanol (2:1), mixed, centrifuged, and supernatant collected. NaCl solution (0.9%) was added, centrifuged, and supernatant dried under nitrogen. Residue was dissolved in 3% Triton X-100 and TG measured using a TG assay kit [1]
.
- **Hepatic FFA Measurement:** Liver tissue (50 mg) was homogenized in PBS, centrifuged at 860×g for 20 min at 4°C. Supernatant protein concentration was measured by BCA assay, and FFA concentration determined using a non-esterified free fatty acids assay kit [1]
.
- **Hepatic Glycogen Measurement:** Liver tissue (50 mg) was homogenized in ice-cold PBS, centrifuged at 14,000×g for 10 min at 4°C. Glycogen concentration in supernatant was measured using an EnzyChrom Glycogen assay kit and normalized to protein concentration [1]
.

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Animals and Diet: Male Sprague-Dawley rats (3 weeks old, 40-60 g) were housed under standard conditions. After 7 days acclimation on standard diet, rats were divided into normal diet group (320 kcal/100 g, 4.65% fat, n=12) and HFD group (500 kcal/100 g, 60% fat, n=28) for 24 weeks [1]
.
- Drug Administration: Octreotide was administered subcutaneously at 40 μg/kg body weight every 12 hours for 8 days to obese rats (body weight ≥1.4-fold higher than controls). HFD-control group received no treatment [1]
.
- Monitoring: Body weight, body length, and tail length were measured weekly. Food intake was monitored daily during octreotide administration [1]
.
- Glucose and Insulin Tolerance Tests: After 12 h fasting, rats received intraperitoneal glucose (2.0 g/kg) or insulin (7.5 U/kg). Blood samples were collected from tail vein at 0, 15, 30, 60, and 120 min post-injection. Glucose levels were measured using a glucometer. AUC was calculated using GraphPad Prism [1]
.
- Sample Collection: At the end of experiment, rats were fasted for 12 h and sacrificed with 2% sodium pentobarbital (45 mg/kg, i.p.). Blood samples were collected, centrifuged at 860×g for 15 min at 4°C, and serum stored at -80°C. Liver tissues were isolated for histological analysis, RNA/protein extraction, or frozen for Oil Red O staining [1]
.
- Lee's Index Calculation: Lee's index = [Body weight (g)¹ᐟ³ × 1000] / body length (cm) [1]
.
- HOMA Index Calculation: HOMA index = [FPG (mmol/L) × fasting serum insulin (μU/mL)] / 22.5 [1]
.
- Liver Histology: Paraffin-embedded liver sections were stained with H&E for morphological evaluation. Frozen liver sections were stained with Oil Red O for lipid assessment. IOD values were analyzed using Image Pro Plus software [1]
.
- Hepatic TG Measurement: Liver tissue (50 mg) was homogenized in chloroform-methanol (2:1), mixed, centrifuged, and supernatant collected. NaCl solution (0.9%) was added, centrifuged, and supernatant dried under nitrogen. Residue was dissolved in 3% Triton X-100 and TG measured using a TG assay kit [1]
.
- Hepatic FFA Measurement: Liver tissue (50 mg) was homogenized in PBS, centrifuged at 860×g for 20 min at 4°C. Supernatant protein concentration was measured by BCA assay, and FFA concentration determined using a non-esterified free fatty acids assay kit [1]
.
- Hepatic Glycogen Measurement: Liver tissue (50 mg) was homogenized in ice-cold PBS, centrifuged at 14,000×g for 10 min at 4°C. Glycogen concentration in supernatant was measured using an EnzyChrom Glycogen assay kit and normalized to protein concentration [1]
.

Absorption, Distribution and Excretion
Octreotide is completely absorbed after subcutaneous injection. After oral administration of sustained-release capsules, the peak concentration is 33% lower than that after subcutaneous injection. The Cmax after oral administration is 1.67–2.5 hours, while that after subcutaneous injection is only 30 minutes. In patients with acromegaly, the peak concentration is 2.5 mg/nL with 20 mg twice daily, and 5.30 ng/mL with 40 mg twice daily. AUC increases proportionally with dose regardless of the route of administration. After oral administration of octreotide, approximately 32% is excreted in the urine, and 30–40% is excreted in the feces via the liver. Approximately 11% of the unchanged drug remains in the urine, and 2% is recovered from the feces. A pharmacokinetic study showed a volume of distribution of 13.6 L in healthy volunteers. Another pharmacokinetic study showed that the volume of distribution after intravenous administration in healthy volunteers ranged from 18.1 to 30.4 L. The systemic clearance of octreotide was 7–10 L/h. One pharmacokinetic study showed that the total clearance of octreotide was 11.4 L/h. Metabolism/Metabolites Octreotide has been reported to be primarily metabolized in the liver. Biological Half-Life The plasma half-life after subcutaneous injection was estimated to be 0.2 hours. The mean elimination half-life between subcutaneous and oral administration was 2.3 to 2.7 hours, with no statistically significant difference. One pharmacokinetic study showed a plasma half-life of 72 to 113 minutes.

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Hepatotoxicity
In a minority of patients receiving octreotide treatment, mild, transient, and asymptomatic elevations in serum transaminase levels may occur; in some patients, transaminase levels remain elevated and worsen over time, potentially requiring discontinuation of the drug. Furthermore, several cases of acute, clinically significant liver injury caused by octreotide have been reported. Liver injury typically occurs within 1 to 6 months of starting treatment, and the incidence may be higher with higher doses. Most cases of liver injury associated with octreotide treatment are asymptomatic and without jaundice, characterized by significantly elevated serum ALT and AST, while serum alkaline phosphatase, GGT, and bilirubin levels are normal or near normal. However, jaundice may occur in some cases, especially after re-administration. There are currently no reports of acute liver failure or bile duct disappearance syndrome associated with octreotide; a characteristic of this injury is rapid improvement after discontinuation of injections or infusions. Several cases of significantly elevated transaminase levels have been reported in neonates and infants with congenital hyperinsulinemia receiving continuous infusion of high-dose octreotide, which rapidly returned to normal upon discontinuation of the drug. Octreotide inhibits gallbladder contraction and reduces bile secretion, and long-term treatment is associated with an increased incidence of high-cholesterol gallstones. Prospective studies have shown that 25% to 65% of acromegaly patients receiving octreotide maintenance therapy develop gallstones (detected by ultrasound), some of whom develop symptomatic gallstones requiring hospitalization and cholecystectomy. Even after cholecystectomy, cholesterol stones can still form in the common bile duct and intrahepatic bile ducts, causing symptoms, sepsis, and even requiring partial hepatectomy. Ursodeoxycholic acid treatment does not appear to prevent gallstone formation during octreotide treatment, although it may be helpful. Octreotide is also associated with acute pancreatitis, possibly due to its inhibitory effect on gastrointestinal hormone release, although other cases may be due to gallstone expulsion and pancreatic duct obstruction. Probability score: C (likely a clinically significant cause of liver damage).

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Effects during pregnancy and lactation
◉ Overview of use during lactation
It has not been studied whether octreotide is excreted into breast milk. However, due to its high molecular weight of 10¹⁹ Daltons, very little is likely excreted into breast milk. It is poorly absorbed orally, but has been safely administered directly to infants by injection, so adverse effects on breastfed infants are unlikely. At least three infants have been successfully breastfed without any reported adverse reactions. Until more data are available, breastfeeding women should use octreotide under close monitoring of their infants, especially if the infant is under 2 months old.
◉ Effects on breastfed infants
One mother received octreotide for acromegaly during pregnancy and postpartum (dosage not specified). She breastfed her infant for 4 months (feeding duration not specified) without any apparent problems.
A woman with acromegaly received long-acting octreotide (Zanderidin LAR; dosage not specified) every 6 weeks postpartum while breastfeeding. Six months postpartum, the injection frequency increased to once every four weeks. She breastfed her infant for 12 months (feeding extent not specified). The child was developing normally at age 5.
◉ Effects on breastfeeding and lactation
A pregnant woman with acromegaly began monthly injections of 10 mg long-acting octreotide at 12 weeks of gestation. After delivery, she continued breastfeeding until 6 weeks postpartum, after which the dose of octreotide LAR needed to be increased to 20 mg per month. She continued to successfully breastfeed while taking octreotide.

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Protein binding
Approximately 65% of the dose is bound to lipoproteins and albumin in plasma.

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Observed Side Effects: During the 8-day treatment period, octreotide-treated rats displayed normal activity and eating behaviors. No obvious signs of discomfort, diarrhea, or steatorrhea were observed [1]
.
- Potential Side Effects (Literature): The discussion mentions that potential side effects of octreotide include gastrointestinal reactions such as anorexia, cramps, steatorrhea, liquid stools, and diarrhea. However, these were not observed in the current study [1]
.

[1]. Effects of octreotide on hepatic glycogenesis in rats with high fat diet?induced obesity. Mol Med Rep. 2017 Jul;16(1):109-118.

[2]. Beneficial effect of combined treatment with octreotide and pasireotide in PCK rats, an orthologous model of human autosomal recessive polycystic kidney disease. PLoS One. 2017 May 18;12(5):e0177934.

[3]. Effects of octreotide on hepatic glycogenesis in rats with high fat diet‑induced obesity. Mol Med Rep. 2017 Jul;16(1):109-118.

Pharmacodynamics
Octreotide mimics the naturally occurring hormone somatostatin. Similar to somatostatin, it inhibits growth hormone and glucagon, and can be used to treat tissue growth disorders and insulin dysregulation in patients with acromegaly. Furthermore, octreotide can alleviate flushing and diarrhea caused by gastrointestinal tumors by reducing visceral blood flow and various gastrointestinal hormones associated with diarrhea. The product label warns that octreotide may reduce gallbladder contractility, bile secretion, and thyroid-stimulating hormone (TSH) release in healthy volunteers. Additionally, there have been reports of decreased vitamin B12 levels in patients receiving octreotide treatment. Patients taking octreotide should have their vitamin B12 levels closely monitored.

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Background and Chemical Identity: Octreotide is a somatostatin analogue with a longer half-life and more robust effects than native somatostatin. Somatostatin is a neurohormone with extensive biological activities, including decreasing insulin and glucagon secretion, inhibiting gastric emptying and gastric acid secretion, and reducing intestinal absorption of nutrients [1]
.
- Previous Studies: Previous research has demonstrated that octreotide promotes weight loss, reduces insulin hypersecretion, and improves metabolic abnormalities in mice with HFD-induced obesity. It also improves metabolism and oxidative stress disorders [1]
.
- Clinical Uses: In clinical medicine, octreotide is widely used for the treatment of acute pancreatitis and gastrointestinal bleeding [1]
.
- Mechanism of Action in Hepatic Glycogenesis: Octreotide improves hepatic glycogen synthesis in HFD-induced obese rats by activating the Akt/GSK3β signaling pathway. It increases phosphorylation of Akt (Ser473) and GSK3β (Ser9), leading to inactivation of GSK3β (which normally inhibits GS) and increased GS mRNA expression. This results in enhanced glycogen synthesis, decreased blood glucose levels, and improved insulin sensitivity [1]
.
- Dual Effects on Obesity and Metabolism: The study demonstrates that octreotide not only reduces body weight and adiposity but also improves hepatic steatosis, glycogen synthesis, and insulin resistance in HFD-induced obese rats, suggesting potential therapeutic applications for obesity and obesity-associated metabolic disorders including NAFLD [1]
.
- Clinical Relevance: The authors suggest that octreotide may be regarded as a novel therapeutic strategy for HFD-induced obesity and obesity-associated metabolic disorders, based on its beneficial effects on glycogen synthesis, glucose homeostasis, and hepatic steatosis [1]
.
- Dosing Information: Octreotide was administered subcutaneously at 40 μg/kg body weight every 12 hours for 8 days. For in vitro studies, a concentration of 10⁻⁸ mmol/L was used [1]
.
- Source: Octreotide used in this study was obtained from Chengdu Tiantai Mountain Pharmaceutical Co., Ltd. (Chengdu, China) [1]
.

C49H66N10O10S2

1019.24

1018.44

C, 57.74; H, 6.53; N, 13.74; O, 15.70; S, 6.29

83150-76-9

Octreotide acetate;79517-01-4;Octreotide pamoate;135467-16-2

448601

White to off-white solid powder

1.4±0.1 g/cm3

1447.2±65.0 °C at 760 mmHg

153-156

829.1±34.3 °C

0.0±0.3 mmHg at 25°C

1.673

0.77

13

14

17

71

1740

10

C[C@H]([C@H]1C(=O)N[C@@H](CSSC[C@@H](C(=O)N[C@H](C(=O)N[C@@H](C(=O)N[C@H](C(=O)N1)CCCCN)CC2=CNC3=CC=CC=C32)CC4=CC=CC=C4)NC(=O)[C@@H](CC5=CC=CC=C5)N)C(=O)N[C@H](CO)[C@@H](C)O)O

DEQANNDTNATYII-OULOTJBUSA-N

InChI=1S/C49H66N10O10S2/c1-28(61)39(25-60)56-48(68)41-27-71-70-26-40(57-43(63)34(51)21-30-13-5-3-6-14-30)47(67)54-37(22-31-15-7-4-8-16-31)45(65)55-38(23-32-24-52-35-18-10-9-17-33(32)35)46(66)53-36(19-11-12-20-50)44(64)59-42(29(2)62)49(69)58-41/h3-10,13-18,24,28-29,34,36-42,52,60-62H,11-12,19-23,25-27,50-51H2,1-2H3,(H,53,66)(H,54,67)(H,55,65)(H,56,68)(H,57,63)(H,58,69)(H,59,64)/t28-,29-,34-,36+,37+,38-,39-,40+,41+,42+/m1/s1

(4R,7S,10S,13R,16S,19R)-10-(4-aminobutyl)-19-[[(2R)-2-amino-3-phenylpropanoyl]amino]-16-benzyl-N-[(2R,3R)-1,3-dihydroxybutan-2-yl]-7-[(1R)-1-hydroxyethyl]-13-(1H-indol-3-ylmethyl)-6,9,12,15,18-pentaoxo-1,2-dithia-5,8,11,14,17-pentazacycloicosane-4-carboxamide

SMS-201-995; Octreotide; Octreotide-LAR; Longastatin; Octreotide acetate; 83150-76-9; Sandostatin; SMS 201-995; Octreotidum; Octreotida; Octreotide-LAR; .

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: (1). Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light.  (2). This product is not stable in solution, please use freshly prepared working solution for optimal results.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~100 mg/mL (~98.11 mM)

Solubility in Formulation 1: 100 mg/mL (98.11 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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 (Please use freshly prepared in vivo formulations for optimal results.)