| Size | Price | Stock | Qty |
|---|---|---|---|
| 2mg |
|
||
| 5mg |
|
||
| 10mg |
|
||
| 25mg |
|
||
| 50mg | |||
| 100mg | |||
| 1g | |||
| Other Sizes |
Semaglutide acetate (NNC-0113-0217; NNC0113-0217), the acetic acid salt form of semaglutide (Ozempic), is a human glucagon-like peptide-1 (GLP-1) receptor agonist with longer duration of antidiabetic action. In order to enhance glycemic control in adults with type 2 diabetes mellitus, the FDA approved semaglutide in December 2017.
| Targets |
GLP-1 receptor
|
|---|---|
| ln Vitro |
Semaglutide is derivatized at lysine 26 and differs from human GLP-1 in two amino acid substitutions (Aib8, Arg34). Semaglutide has an affinity for GLP-1R of 0.38±0.06 nM[1]. With a 94% sequence homology to human GLP-1, semaglutide is an analogue of GLP-1[3].
|
| ln Vivo |
Semaglutide has an MRT of 63.6 hours after s.c. dosing to mini-pigs and a plasma half-life of 46 hours in mini-pigs after intravenous administration[1]. Motor impairments caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) are ameliorated by semaglutide. Semaglutide also protects dopaminergic neurons in the substantia nigra and striatum by rescuing the decrease in tyrosine hydroxylase (TH) levels, reducing lipid peroxidation, alleviating inflammation, inhibiting the apoptosis pathway, and increasing the expression of autophagy-related proteins. Furthermore, semaglutide, the long-acting GLP-1 analogue, outperforms NN-2211 in the majority of parameters[2].
|
| Enzyme Assay |
HEK293‐SNAP‐GLP‐1R cells were labelled in suspension with SNAP‐Lumi4‐Tb (40 nM, Cisbio, Codelet, France) for 1 hour at room temperature in complete medium. After washing and resuspension in hanks' balanced salt solution containing 0.1% bovine serum albumin and metabolic inhibitors (20 mmol/L 2‐deoxygucose and 10 mmol/L NaN3) to prevent GLP‐1R internalization, binding experiments were performed by time‐resolved förster resonance energy transfer (FRET) using exendin (9‐39) with fluorescein isothiocyanate (FITC) installed at position K12 as previously described. [4]
|
| Cell Assay |
Semaglutide activates the GLP-1 receptor in pancreatic beta cells leading to glucose-dependent insulin release. It also decreases glucagon secretion, slows gastric emptying, and promotes satiety.
|
| Animal Protocol |
Mice: Male C57BL/6 mice 10 weeks old (20-25 g) are used throughout the study. Six groups of mice are randomly assigned (n = 12 per group). The treatments were as follows: (i) saline alone was given to the control group; (ii) NN-2211 group received saline and NN-2211 (25 nmol/kg ip. once daily for 7 days); (iii) Semaglutide group received saline and Semaglutide (25 nmol/kg ip. once daily for 7 days); (iv) MPTP group received MPTP alone (once daily 20 mg/kg ip. for 7 days); (v) MPTP (once daily 20 mg/kg ip. for 7 days) was immediately followed by NN-2211 treated group (25 nmol/kg ip. once daily for 7 days). (vi) MPTP (20 mg/kg i.p. once daily for 7 days), which was immediately followed by the group treated with semaglutide (25 nmol/kg i.p. once daily for 7 days). Measure behavioral changes, neuronal damage, inflammatory markers, and other biomarkers at the conclusion of drug treatments[2].
|
| ADME/Pharmacokinetics |
Absorption: In a clinical trial, semaglutide's Cmax was 10.9 nmol/L, AUC was 3123.4 nmol·h/L, and Tmax was 56 h, achieved within 1-3 days. Absolute bioavailability was 89%. Steady-state concentrations of oral tablets were reached within 4-5 weeks. The mean steady-state concentration of semaglutide refers to the mean steady-state concentration after administration of a dose from 0.5 mg to 1 mg, ranging from 16 nmol/L to 30 nmol/L. Elimination pathway: The drug is primarily cleared by the kidneys and can be excreted in urine and feces. The primary elimination route is urine, accounting for approximately 53% of the ingested radiolabeled dose, followed by feces, accounting for approximately 18.6%. A small amount (3.2%) is excreted via exhalation. Hepatic impairment does not appear to affect the drug's clearance, and no dose adjustment is required for patients with impaired hepatic function. Volume of distribution: Semaglutide has a volume of distribution of 8 to 9.4 liters. It crosses the rat placenta.
Clearance: According to a clinical study, the clearance of semaglutide is 0.039 L/h. The FDA label indicates that the clearance of semaglutide in patients with type 2 diabetes is approximately 0.05 L/h. Metabolism/Metabolites: Semaglutide is cleaved at the peptide backbone, followed by β-oxidation of the fatty acid chain. Naturally occurring GLP-1 is rapidly metabolized by dipeptidyl peptidase-4 (DPP-4) and other enzymes widely present in human tissues. Chemical modifications make semaglutide less susceptible to degradation by gastrointestinal DPP-4 enzymes. It is metabolized slowly and extensively, with approximately 83% of the administered dose remaining in plasma as the parent drug. Neuroendopeptidase (NEP) is another enzyme that metabolizes this drug. DPP-4 inactivates semaglutide by cleaving the N-terminal fragment, while NEP hydrolyzes peptide bonds. Six distinct semaglutide metabolites have been identified in human plasma. The major metabolite, P3, accounts for approximately 7.7% of the ingested dose. Biological Half-Life: One of the main characteristics of semaglutide is its long half-life of 168 hours. This long half-life is attributed to its binding to albumin. This reduces renal clearance and protects semaglutide from metabolic degradation. |
| Toxicity/Toxicokinetics |
Hepatotoxicity
In large clinical trials, the incidence of elevated serum enzymes was not higher in the semaglutide treatment group compared to placebo or control drugs, and no clinically significant cases of liver injury were reported. In fact, semaglutide and other GLP-1 analogues often improve serum transaminase levels (and hepatic steatosis), making it a potential treatment for non-alcoholic fatty liver disease. Since its market launch, no case reports of hepatotoxicity caused by semaglutide have been published, and liver injury is not listed as an adverse event in the product information leaflet. Therefore, if liver injury caused by semaglutide occurs, it must be extremely rare. Probability score: E (unlikely to cause clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation There is currently no information on the clinical use of semaglutide during lactation. Because semaglutide is a peptide molecule with a molecular weight of 4113 Daltons and a protein binding rate of over 99%, its content in breast milk is likely to be very low. The likelihood of infants absorbing this drug is also very low, as it is likely to be destroyed in the infant's gastrointestinal tract. Until more data is available, breastfeeding women should use semaglutide with caution, especially when breastfeeding newborns or premature infants. ◉ Effects on breastfed infants No published information found as of the revision date. ◉ Effects on lactation and breast milk No published information found as of the revision date. View more◈ What is semaglutide? Protein Binding Semaglutide binds to plasma albumin with high affinity, ensuring high drug stability. Its binding rate to albumin exceeds 99%. |
| References |
[1]. Semaglutide and Cardiovascular Outcomes in Patients with Type 2 Diabetes. N Engl J Med. 2016 Nov 10;375(19):1834-1844.
[3]. Semaglutide: First Global Approval. Drugs. 2018 Feb;78(2):275-284.
[4]. In vivo and in vitro characterization of GL0034, a novel long‐acting glucagon‐like peptide‐1 receptor agonist. Diabetes Obes Metab. 2022 Nov; 24(11): 2090–2101. |
| Additional Infomation |
Novo Nordisk has developed a subcutaneous formulation of semaglutide (Ozempic®), a modified human glucagon-like peptide-1 (GLP-1) analog for the treatment of type 2 diabetes. Developed using Novo Nordisk's proprietary protein acylation technology, the drug is administered via an injection device. Semaglutide lowers blood sugar by stimulating insulin release, while also promoting weight loss. The once-weekly subcutaneous injection of semaglutide was recently approved in the United States, Puerto Rico, and Canada, and has received a positive opinion in the European Union for the treatment of type 2 diabetes. The drug will be marketed as a pre-filled Ozempic® Pen. Semaglutide is also currently under regulatory review in Japan and Switzerland for the treatment of type 2 diabetes. Clinical development for obesity, non-alcoholic steatohepatitis (NAHH), and non-alcoholic fatty liver disease (NAFLD) is underway globally. This article summarizes the key milestones in the development of semaglutide, culminating in its first approval for the treatment of type 2 diabetes. [3]
In patients with type 2 diabetes at high cardiovascular risk, the incidence of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke was significantly lower in patients treated with semaglutide than in patients treated with placebo, confirming the non-inferiority of semaglutide. [2] Semaglutide is a polypeptide composed of 31 amino acids linked by peptide bonds. It is an agonist of glucagon-like peptide-1 receptor (GLP-1 AR) and is used to treat type 2 diabetes. It has multiple effects, including hypoglycemic, glucagon-like peptide-1 receptor agonist, anti-obesity, neuroprotective, and appetite-suppressing effects. It is a polypeptide and lipopeptide. Semaglutide is a glucagon-like peptide-1 (GLP-1) analog used to treat type 2 diabetes and requires lifestyle modifications, such as dietary restrictions and increased physical activity. Other members of this class of drugs include exenatide and liraglutide. Semaglutide, developed by Novo Nordisk, was approved by the U.S. Food and Drug Administration (FDA) for subcutaneous injection in December 2017. Tablets were approved for oral administration in September 2019. Semaglutide works by binding to and activating the GLP-1 receptor, thereby stimulating insulin secretion and lowering blood sugar. Subcutaneous injection is administered once weekly, and tablets once daily. Semaglutide has a competitive advantage compared to other diabetes treatments that may require multiple daily doses. Clinical trials have shown that the drug reduces glycated hemoglobin (HbA1c) levels and promotes weight loss in patients with type 2 diabetes. In June 2021, the FDA approved semaglutide for the treatment of chronic weight management in obese or overweight adults with at least one weight-related disease, the first drug approved for this purpose since 2014. Health Canada and the European Medicines Agency (EMA) have also approved semaglutide for weight management. On May 31, 2023, the FDA issued a warning regarding the use of semaglutide after receiving an adverse event report. The safety and efficacy of salt forms of semaglutide, including semaglutide sodium and semaglutide acetate, have not been established. View MoreSemaglutide is a GLP-1 receptor agonist. The mechanism of action of semaglutide is as a glucagon-like peptide-1 (GLP-1) receptor agonist. Smegglutide is a recombinant DNA-produced polypeptide, an analogue of human glucagon-like peptide-1 (GLP-1), used in combination with diet and exercise to treat type 2 diabetes, either alone or in combination with other antidiabetic drugs. There are currently no reports of hepatotoxicity associated with smegglutide treatment. Smegglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist with 94% homology to human GLP-1 (7-37), and has hypoglycemic and appetite-regulating effects. After administration, smegglutide binds to and activates the GLP-1 receptor. In pancreatic β-cells, this increases glucose-dependent insulin release. Smegglutide reduces elevated glucagon secretion by inhibiting pancreatic α-cells and delays gastric emptying. These effects collectively lower postprandial blood glucose levels. In the brain, smegglutide binds to and activates the GLP-1 receptor, thereby suppressing appetite, reducing calorie intake, and decreasing weight. GLP-1 is normally secreted by L cells in the gastrointestinal mucosa after meals to normalize blood glucose levels. It also plays an important role in regulating appetite and calorie intake. Smegglutide is indicated for improving glycemic control in adults with type 2 diabetes and as an adjunct to diet and exercise. However, smegglutide is not a first-line treatment for diabetic patients whose blood glucose cannot be controlled by diet and exercise. Furthermore, it has not been studied in patients with pancreatitis. Smegglutide is not indicated for patients with type 1 diabetes or for the treatment of diabetic ketoacidosis. Smegglutide is indicated for long-term weight management in obese or overweight adults with at least one weight-related condition (e.g., hypertension, type 2 diabetes, or high cholesterol), requiring a low-calorie diet and increased physical activity. Smegglutide is also indicated for long-term weight management in children aged 12 years and older with an initial BMI at or above the 95th percentile for their age and sex. Smegglutide can reduce glycated hemoglobin (HbA1c), systolic blood pressure, and body weight. After 12 weeks of treatment, semaglutide lowers fasting and postprandial blood glucose by increasing insulin secretion and decreasing glucagon secretion (glucagon secretion is typically associated with elevated blood glucose). Semaglutide also lowers fasting triglycerides and very low-density lipoprotein cholesterol (VLDL-C), thus having a beneficial effect on cardiovascular health. Studies have shown that semaglutide can induce medullary thyroid carcinoma in rodents. Although its clinical significance in humans is unclear, the FDA recommends that patients with a personal or family history of medullary thyroid carcinoma should not use this drug. Semaglutide also carries the risk of pancreatitis and dehydration. Patients must maintain adequate hydration while taking semaglutide, and if abdominal pain radiating to the back occurs, immediate medical attention is recommended. Because this drug delays gastric emptying, the efficacy or adverse reactions of other oral medications must be monitored.Mechanism of Action: Glucose Control Mechanism GLP-1 is a physiological hormone that promotes glycemic control through multiple mechanisms, including promoting insulin secretion, delaying gastric emptying, and reducing postprandial glucagon secretion. Glucose homeostasis depends on hormones such as insulin and amylin, which are secreted by pancreatic β-cells. Semaglutide has 94% similarity to human GLP-1. Analogs of this hormone, such as semaglutide, stimulate insulin synthesis by stimulating pancreatic islet cells and reducing glucagon secretion. They selectively bind directly to GLP-1 receptors, producing a variety of beneficial downstream effects, lowering blood glucose in a glucose-dependent manner. Mechanisms of Cardiovascular Benefits and Weight Loss In hypercholesterolemia, semaglutide is thought to slow the progression of atherosclerosis by reducing intestinal permeability and inflammation. Weight loss is thought to be due to decreased appetite and food cravings after semaglutide administration. Hepatotoxicity: In large clinical trials, the incidence of elevated serum enzymes was not higher in the semaglutide treatment group than in the placebo or control groups, and no clinically manifested cases of liver injury were reported. In fact, treatment with semaglutide and other GLP-1 analogs often improves serum transaminase levels (and hepatic steatosis), making it a potential treatment for non-alcoholic fatty liver disease. Since its market launch, there have been no reported cases of hepatotoxicity caused by semaglutide, and liver injury is not listed as an adverse reaction in the product information leaflet. Therefore, even if liver injury caused by semaglutide occurs, it must be extremely rare. |
| Molecular Formula |
C189H295N45O61
|
|---|---|
| Molecular Weight |
4173.693
|
| Exact Mass |
4173.14
|
| Elemental Analysis |
C, 52.58; H, 7.62; N, 19.51; O, 20.29
|
| CAS # |
1997361-85-9
|
| Related CAS # |
910463-68-2 (Semaglutide free base); 2924330-56-1 (sodium)
|
| PubChem CID |
162393099
|
| Sequence |
H-His-Aib-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Val-Ser-Ser-Tyr-Leu-Glu-Gly-Gln-Ala-Ala-Lys-Glu-Phe-Ile-Ala-Trp-Leu-Val-Arg-Gly-Arg-Gly-OH
|
| SequenceShortening |
HXEGTFTSDV SSYLEGQAAK EFIAWLVRGR G
|
| Appearance |
White to off-white solid powder
|
| LogP |
-5.8
|
| Hydrogen Bond Donor Count |
58
|
| Hydrogen Bond Acceptor Count |
65
|
| Rotatable Bond Count |
151
|
| Heavy Atom Count |
295
|
| Complexity |
9620
|
| Defined Atom Stereocenter Count |
30
|
| SMILES |
CC[C@H](C)[C@@H](C(=O)N[C@@H](C)C(=O)N[C@@H](CC1=CNC2=CC=CC=C21)C(=O)N[C@@H](CC(C)C)C(=O)N[C@@H](C(C)C)C(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)N[C@@H](CCCNC(=N)N)C(=O)NCC(=O)O)NC(=O)[C@H](CC3=CC=CC=C3)NC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CCCCNC(=O)COCCOCCNC(=O)COCCOCCNC(=O)CC[C@@H](C(=O)O)NC(=O)CCCCCCCCCCCCCCCCC(=O)O)NC(=O)[C@H](C)NC(=O)[C@H](C)NC(=O)[C@H](CCC(=O)N)NC(=O)CNC(=O)[C@H](CCC(=O)O)NC(=O)[C@H](CC(C)C)NC(=O)[C@H](CC4=CC=C(C=C4)O)NC(=O)[C@H](CO)NC(=O)[C@H](CO)NC(=O)[C@H](C(C)C)NC(=O)[C@H](CC(=O)O)NC(=O)[C@H](CO)NC(=O)[C@H]([C@@H](C)O)NC(=O)[C@H](CC5=CC=CC=C5)NC(=O)[C@H]([C@@H](C)O)NC(=O)CNC(=O)[C@H](CCC(=O)O)NC(=O)C(C)(C)NC(=O)[C@H](CC6=CNC=N6)N.CC(=O)O
|
| InChi Key |
CQZWIAQBGGIDHL-GENFIEAASA-N
|
| InChi Code |
InChI=1S/C187H291N45O59.C2H4O2/c1-18-105(10)154(180(282)208-108(13)159(261)216-133(86-114-89-200-119-50-40-39-49-117(114)119)170(272)218-129(82-102(4)5)171(273)228-152(103(6)7)178(280)215-121(53-44-72-199-186(192)193)162(264)201-91-141(242)209-120(52-43-71-198-185(190)191)161(263)204-94-151(257)258)230-172(274)131(83-111-45-33-31-34-46-111)219-167(269)126(64-69-149(253)254)214-166(268)122(51-41-42-70-195-144(245)98-290-79-78-289-76-74-197-145(246)99-291-80-77-288-75-73-196-139(240)66-61-127(183(285)286)211-140(241)54-37-29-27-25-23-21-19-20-22-24-26-28-30-38-55-146(247)248)212-158(260)107(12)206-157(259)106(11)207-165(267)125(60-65-138(189)239)210-142(243)92-202-163(265)123(62-67-147(249)250)213-168(270)128(81-101(2)3)217-169(271)130(85-113-56-58-116(238)59-57-113)220-175(277)135(95-233)223-177(279)137(97-235)224-179(281)153(104(8)9)229-174(276)134(88-150(255)256)221-176(278)136(96-234)225-182(284)156(110(15)237)231-173(275)132(84-112-47-35-32-36-48-112)222-181(283)155(109(14)236)227-143(244)93-203-164(266)124(63-68-148(251)252)226-184(287)187(16,17)232-160(262)118(188)87-115-90-194-100-205-115;1-2(3)4/h31-36,39-40,45-50,56-59,89-90,100-110,118,120-137,152-156,200,233-238H,18-30,37-38,41-44,51-55,60-88,91-99,188H2,1-17H3,(H2,189,239)(H,194,205)(H,195,245)(H,196,240)(H,197,246)(H,201,264)(H,202,265)(H,203,266)(H,204,263)(H,206,259)(H,207,267)(H,208,282)(H,209,242)(H,210,243)(H,211,241)(H,212,260)(H,213,270)(H,214,268)(H,215,280)(H,216,261)(H,217,271)(H,218,272)(H,219,269)(H,220,277)(H,221,278)(H,222,283)(H,223,279)(H,224,281)(H,225,284)(H,226,287)(H,227,244)(H,228,273)(H,229,276)(H,230,274)(H,231,275)(H,232,262)(H,247,248)(H,249,250)(H,251,252)(H,253,254)(H,255,256)(H,257,258)(H,285,286)(H4,190,191,198)(H4,192,193,199);1H3,(H,3,4)/t105-,106-,107-,108-,109+,110+,118-,120-,121-,122-,123-,124-,125-,126-,127-,128-,129-,130-,131-,132-,133-,134-,135-,136-,137-,152-,153-,154-,155-,156-;/m0./s1
|
| Chemical Name |
acetic acid;18-[[(1S)-4-[2-[2-[2-[2-[2-[2-[[(5S)-5-[[(2S)-2-[[(2S)-2-[[(2S)-5-amino-2-[[2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S)-2-[[(2S,3R)-2-[[(2S)-2-[[(2S,3R)-2-[[2-[[(2S)-2-[[2-[[(2S)-2-amino-3-(1H-imidazol-4-yl)propanoyl]amino]-2-methylpropanoyl]amino]-4-carboxybutanoyl]amino]acetyl]amino]-3-hydroxybutanoyl]amino]-3-phenylpropanoyl]amino]-3-hydroxybutanoyl]amino]-3-hydroxypropanoyl]amino]-3-carboxypropanoyl]amino]-3-methylbutanoyl]amino]-3-hydroxypropanoyl]amino]-3-hydroxypropanoyl]amino]-3-(4-hydroxyphenyl)propanoyl]amino]-4-methylpentanoyl]amino]-4-carboxybutanoyl]amino]acetyl]amino]-5-oxopentanoyl]amino]propanoyl]amino]propanoyl]amino]-6-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-5-carbamimidamido-1-[[2-[[(2S)-5-carbamimidamido-1-(carboxymethylamino)-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-1-oxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-6-oxohexyl]amino]-2-oxoethoxy]ethoxy]ethylamino]-2-oxoethoxy]ethoxy]ethylamino]-1-carboxy-4-oxobutyl]amino]-18-oxooctadecanoic acid
|
| Synonyms |
Semaglutide acetate; Semaglutide (acetate); Semaglutide Acetate; Semalgutide Acetate; BS181345
|
| HS Tariff Code |
2934.99.9001
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
DMSO: >50 mg/mL
Water: >50 mg/mL |
|---|---|
| Solubility (In Vivo) |
Note: Please refer to the "Guidelines for Dissolving Peptides" section in the 4th page of the "Instructions for use" file (upper-right section of this webpage) for how to dissolve peptides. 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. Injection Formulations
Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)(e.g. IP/IV/IM/SC) *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). View More
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)] Oral Formulations
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). View More
Oral Formulation 3: Dissolved in PEG400 (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 0.2396 mL | 1.1980 mL | 2.3960 mL | |
| 5 mM | 0.0479 mL | 0.2396 mL | 0.4792 mL | |
| 10 mM | 0.0240 mL | 0.1198 mL | 0.2396 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT05649137 | Active Recruiting |
Drug: Semaglutide Drug: Placebo |
Obesity Diabetes Mellitus, Type 2 |
Novo Nordisk A/S | January 4, 2023 | Phase 3 |
| NCT05646706 | Active Recruiting |
Drug: Semaglutide Drug: Placebo |
Obesity | Novo Nordisk A/S | January 4, 2023 | Phase 3 |
| NCT05302596 | Active Recruiting |
Drug: Semaglutide Pen Injector |
Obesity Aging |
State University of New York at Buffalo |
September 1, 2022 | Phase 4 |
| NCT05564117 | Active Recruiting |
Drug: Semaglutide Drug: Placebo semaglutide |
Overweight Obesity |
Novo Nordisk A/S | October 11, 2022 | Phase 3 |
| NCT04560998 | Active Recruiting |
Drug: Semaglutide Drug: Placebo (semaglutide) |
Diabetes Mellitus, Type 2 Peripheral Arterial Disease |
Novo Nordisk A/S | October 1, 2020 | Phase 3 |
|
|
|
|
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
