SSTR2/3/5

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).

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].

Western Blot analysis [2]
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.

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]

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

CAM2029 is a new ready-to-use, long-acting octreotide formulation being developed for the long-term treatment of acromegaly, carcinoid syndrome and vasoactive intestinal peptide (VIP)-producing tumours. CAM2029 was found to provide long-acting release of octreotide resulting in a statistically significant suppression of a clinical biomarker insulin-like growth factor 1 (IGF-1) over the target one-month therapeutic period.

1090.3938

C, 53.89; H, 6.28; Cl, 6.49; N, 12.83; O, 14.65; S, 5.87

1607842-55-6

3150-76-979517-01-4 (acetate)135467-16-2 (pamoate); 1607842-55-6 (HCl)

Typically exists as solid at room temperature

PPJMKGDKFBCNIY-LODIGNQBSA-N

InChI=1S/C49H66N10O10S2.2ClH/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);2*1H/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;dihydrochloride

Octreotide hydrochloride, (-)-Octreotide hydrochloride; Octreotide dihydrochloride; Octreotide hydrochloride, (-)-; Octreotide hydrochloride [USAN]; 1607842-55-6; UNII-H92K6Q47Q9; H92K6Q47Q9; Octreotide HCl

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

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

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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