GLP-1 receptor

Albiglutide lowers blood sugar levels after a single dosage in less than 24 hours due to the molecule's binding to the GLP-1 receptor. It is dose-related that both postprandial and fasting glucose levels decrease. Less powerful than GLP-1 is albiglutide. Increased β-cell mass is stimulated by albiglutide administration in animal models of diabetes. Patients with type 2 diabetes experience a maximum concentration in 3-5 days and a half-life of 3.6–6.8 days after receiving a single 30-mg dose SC. 8.2-18.5 L was the apparent volume of distribution following an albiglutide dose. In the bloodstream, albiglutide eventually breaks down into discrete amino acids and small peptides. Albiglutide did not appear to have any effect on respiratory function, heart rate, electrocardiographic intervals, cardiovascular function, or any indication of arrhythmias or abnormalities in the electrocardiograms of male cynomolgus monkeys. Additionally, no effects of albiglutide were observed on neurobehavioral functional assessments. Albiglutide is unable to enter the brain's satiety centers through the blood–brain barrier. After myocardial I/R injury, albiglutide decreased the size of the myocardial infarct and improved cardiac function and energetics. These effects are linked to increased myocardial glucose uptake and a change toward a more energetically favorable substrate metabolism by raising both glucose and lactate oxidation.

Absorption, Distribution and Excretion
Following a single 30 mg dose of abiglutide, maximum concentrations are reached 3 to 5 days post-administration. The mean peak concentration (Cmax) and mean area under the time-concentration curve (AUC) of abiglutide are 1.74 mcg/mL and 465 mcg·h/mL, respectively.
11 L.
67 mL/h.
/Breast milk/ It is unclear whether abiglutide is distributed into human breast milk….
Abiglutide is a glucagon-like peptide-1 analogue, composed of tandemly modified human glucagon-like peptide-1 (7-36) coupled with recombinant human serum albumin, and is approved for the treatment of type 2 diabetes in adults. After subcutaneous injection, abiglutide is primarily absorbed via the lymphatic system, reaching maximum plasma concentrations in 3 to 5 days; steady-state plasma concentrations are reached approximately 4 to 5 weeks after weekly administration. The elimination half-life of abiglutide is approximately 5 days. The clearance rate of abiglutide is 67 mL/h, with an inter-individual variability of 34.9%; no covariates requiring dose adjustment of abiglutide have been identified. Abiglutide lowers fasting blood glucose and reduces postprandial blood glucose fluctuations. Furthermore, abiglutide enhances β-cell secretion when blood glucose is elevated and inhibits β-cell secretion when blood glucose is low; abiglutide does not affect the α-cell response to hypoglycemia. Abiglutide does not prolong the corrected QT interval, but has a slight effect on heart rate in patients with type 2 diabetes. Dose adjustment is not recommended for patients with renal impairment, but experience with patients with severe renal impairment is very limited, and caution is advised in the use of abiglutide in these patients due to the higher incidence of diarrhea, nausea, and vomiting. No clinically significant drug interactions have been observed in clinical trials. In patients with type 2 diabetes, the maximum concentration is reached 3 to 5 days after a single subcutaneous injection of 30 mg abiglutide. Following a single 30 mg injection of abiglutide in patients with type 2 diabetes, the mean peak concentration (Cmax) and mean area under the concentration-time curve (AUC) of abiglutide were 1.74 mcg/mL and 465 mcg·h/mL, respectively. Steady-state exposure was achieved after once-weekly administration for 4 to 5 weeks. Drug exposure in the 30 mg and 50 mg dose groups increased proportionally with the dose. Similar exposures were achieved with subcutaneous injections of abiglutide into the abdomen, thigh, or upper arm. The absolute bioavailability of abiglutide following subcutaneous injection has not been evaluated. The mean estimated volume of distribution after subcutaneous injection of abiglutide was 11 L. Because abiglutide is an albumin fusion molecule, its plasma protein binding has not been evaluated. The mean apparent clearance of abiglutide was 67 mL/hr, and the elimination half-life was approximately 5 days, making once-weekly administration suitable.
Metabolism/Metabolites
Biotransformation studies have not been conducted. Because abiglutide is an albumin fusion protein, its metabolic pathway is likely similar to that of natural human serum albumin, primarily being catabolized in vascular endothelial cells. Abiglutide is a protein, and its expected metabolic pathway involves degradation into small peptides and individual amino acids by ubiquitous proteolytic enzymes. Classical biotransformation studies have not yet been conducted. Biological half-life: 4-7 days. Following subcutaneous injection, the elimination half-life of abiglutide is 5 days; therefore, this drug is suitable for once-weekly administration.

Toxicity Summary
Identification and Use: Albiglutide (trade name: Tanzeum) is a prescription drug approved for improving glycemic control in adults with type 2 diabetes. Human Exposure and Toxicity: Epidemiological meta-analyses have observed pancreatitis and thyroid cancer, but it is unclear whether they are related to treatment. Other adverse events include gastrointestinal symptoms (nausea, vomiting, and diarrhea) and hypoglycemia. Post-marketing reports have shown acute renal failure and exacerbations of chronic renal failure in patients treated with GLP-1 receptor agonists, sometimes requiring hemodialysis. Some of these events occurred in patients without known underlying kidney disease. The risk of hypoglycemia increases when abiglutide is used in combination with insulin secretagogues (such as sulfonylureas) or insulin. Albiglutide has been reported to be associated with acute pancreatitis in clinical trials. Patients treated with abiglutide may have an increased risk of thyroid C-cell tumors. Albiglutide is a GLP-1 receptor agonist that enhances glucose-dependent insulin secretion. Albiglutide also delays gastric emptying. Animal studies: The carcinogenicity of abiglutide in rodents could not be assessed, but other glucagon-like peptide-1 (GLP-1) receptor agonists induced thyroid C-cell tumors in rodents at clinically relevant exposure doses. The relevance of GLP-1 receptor agonist-induced C-cell tumors in rodents to humans has not been determined. In pregnant mice that received subcutaneous injections of the drug on days 6 to 15 of gestation (organogenesis), in addition to maternal toxicity (weight loss and reduced food intake), embryo-fetal death (post-implantation loss) and rib curvature (wavy) were observed. Offspring exhibited weight loss, dehydration, and hypothermia before weaning, as well as delayed prepuce-glans separation. Increased mortality and morbidity were observed in lactating females at all doses. Reduced weight gain in pups was also observed during treatment. In mouse fertility studies, reduced estrous cycles were observed at a dose of 50 mg/kg/day, which was associated with maternal toxicity (weight loss and reduced food intake). Female mice were treated with subcutaneous injections 7 days before mating with males and continued until mating. Reduced estrous cycles were observed. Hepatotoxicity: In large clinical trials, the incidence of elevated serum enzymes in the abiglutide treatment group was not higher than in the placebo or control groups, and no clinically significant liver injury cases were reported. Since its market launch, no cases of abiglutide-induced hepatotoxicity have been reported, and liver injury is not listed as an adverse event in the product information leaflet. Therefore, even if abiglutide-induced liver injury occurs, it is certainly very rare. Probability Score: E (Unlikely to be the cause of clinically significant liver injury). Drug Interactions: Potential pharmacokinetic interactions (absorption alterations due to slowed gastric emptying caused by abiglutide). In clinical trials, abiglutide did not have any clinically relevant effect on the absorption of concurrently administered oral medications. However, caution should be exercised when abiglutide is used in combination with oral medications. This article reviews studies on the interactions between glucagon-like peptide-1 receptor agonists (GLP-1RAs) and oral medications. We searched the PubMed database (up to December 5, 2011) using the keywords exenatide, liraglutide, abiglutide, and lixilatide. Results showed that exenatide administration decreased the AUC of acetaminophen and lovastatin; liraglutide administration decreased the AUC of lisinopril and digoxin. In 10 studies, GLP-1RAs decreased the Cmax of the study drug; in 14 studies, GLP-1RAs prolonged the tmax of the study drug. Differences in drug pharmacokinetic properties and study design may explain the differences in interaction potential. GLP-1RAs may have clinically significant interactions with drugs requiring target peak concentrations or rapid onset of action. Further studies in patients with type 2 diabetes are needed to further evaluate and compare the effects of several GLP-1RAs on the steady-state pharmacokinetics and pharmacodynamics of concomitant oral medications.

[1]. Expert Opin Biol Ther . 2016 Dec;16(12):1557-1569.

Albiglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist biologic agent used to treat type 2 diabetes. It is marketed by GlaxoSmithKline (GSK) under the brand names Eperzan and Tanzeum. Albiglutide is a human serum albumin-fused, dipeptidyl peptidase-4 (DPP-4)-resistant glucagon-like peptide-1 dimer. Albiglutide received FDA approval on April 15, 2014. Albiglutide is a recombinant DNA-produced peptide analog of human glucagon-like peptide-1 (GLP-1) that can be used alone or in combination with other antidiabetic drugs, in conjunction with diet and exercise, to treat type 2 diabetes. There are currently no published reports of hepatotoxicity associated with albiglutide treatment. Albiglutide is a long-acting glucagon-like peptide-1 (GLP-1) receptor agonist with hypoglycemic activity. Albiglutide is a product of the fusion of GLP-1 (7-36) dimer and recombinant human serum albumin. After subcutaneous injection, the drug has a half-life of 4-7 days and is not readily degraded by dipeptidyl peptidase-4 (DPP-4).
See also: Albiglutide (note moved to).

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Drug Indications
Indicated as adjunctive therapy to improve glycemic control in adult patients with type 2 diabetes.
Epuzan is indicated for the treatment of type 2 diabetes in adults to improve glycemic control, specifically as follows: Monotherapy: When diet and exercise alone are insufficient to adequately control glycemia, and metformin is unsuitable due to contraindications or intolerance. Additional combination therapy: When other hypoglycemic agents, such as basal insulin, combined with diet and exercise, fail to provide adequate glycemic control, it may be used in combination with other hypoglycemic agents (see Sections 4.4 and 5.1 for available data on different combination therapy regimens).
Treatment of Type II Diabetes

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Mechanism of Action
Abiglutide is a GLP-1 (glucagon-like peptide-1) receptor agonist that enhances glucose-dependent insulin secretion. Abiglutide also delays gastric emptying.
Tanzem is a GLP-1 receptor agonist that enhances glucose-dependent insulin secretion. Tanzem also delays gastric emptying.

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Therapeutic Uses
Incretins; Antidiabetic Drugs
/Clinical Trials/ ClinicalTrials.gov is a registry and results database that includes publicly and privately funded human clinical studies worldwide. This website is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each record on ClinicalTrials.gov provides a summary of the study protocol, including: the disease or condition; the intervention (e.g., the medical product, behavior, or procedure being investigated); the title, description, and design of the study; participation requirements (eligibility criteria); the location of the study; contact information for the study location; and links to relevant information from other health websites, such as NLM's MedlinePlus (which provides patient health information) and PubMed (which provides citations and abstracts of academic articles in the medical field). Albiglutide is indexed in this database. Tanzeum is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes. /Included in US product label/
Experimental treatment: Rats were treated with alphaglutide followed by 30 minutes of myocardial ischemia, followed by 24 hours of reperfusion. Left ventricular infarction area, hemodynamics, function, and energy metabolism were measured. Cardiac glucose utilization, carbohydrate metabolism, and metabolic gene expression were also evaluated. Albiglutide significantly reduced infarct area and simultaneously improved post-ischemic hemodynamic, cardiac function, and energy metabolism parameters. Albiglutide significantly increases cardiac glucose uptake both in vivo and in vitro, while reducing lactate efflux. Direct analysis of metabolic substrate utilization in the heart showed that abiglutide increased the relative oxidation rates of carbohydrates and fats, partly due to increased oxidation of both glucose and lactate. Metabolic gene expression analysis showed that abiglutide upregulated the expression of key glucose metabolism genes in non-ischemic myocardium. Albiglutide reduced myocardial infarction area and improved cardiac function and energy metabolism following myocardial ischemia/reperfusion injury.

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Drug Warning
/Black Box Warning/ Tanzem is contraindicated in patients with a personal or family history of medullary thyroid carcinoma (MTC) or multiple endocrine neoplasia type 2 (MEN 2). Patients should be informed of the potential risk of MTC with tanzem and of any symptoms of thyroid tumors (e.g., neck mass, dysphagia, dyspnea, persistent hoarseness). The value of routine monitoring of serum calcitonin or thyroid ultrasound in the early detection of medullary thyroid carcinoma (MTC) in patients receiving tanzem is uncertain. /Warning/ The carcinogenicity of abiglutide in rodents cannot be assessed, but other glucagon-like peptide-1 (GLP-1) receptor agonists have caused thyroid C-cell tumors in rodents at clinically relevant exposure levels. The relevance of GLP-1 receptor agonist-induced C-cell tumors in rodents to humans has not been established. It is currently unknown whether tanzeum causes thyroid C-cell tumors, including medullary thyroid carcinoma (MTC), in humans. Post-marketing reports have shown acute renal failure and exacerbations of chronic renal failure in patients treated with GLP-1 receptor agonists, sometimes requiring hemodialysis. Some of these events occurred in patients without known underlying kidney disease. Caution should be exercised when initiating or increasing the dose of tanzeum in patients with renal impairment. Severe hypersensitivity reactions (pruritus, rash, dyspnea) have been reported in patients treated with abiglutide. ¹If a hypersensitivity reaction occurs, abiglutide should be discontinued and the patient treated according to standard treatment protocols, and closely monitored until symptoms subside.
For more complete data on drug warnings for abiglutide (14 in total), please visit the HSDB record page.

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The chemical structure of abiglutide is distinct from other marketed GLP-1 receptor agonists. It has fewer gastrointestinal side effects and is safe for patients with renal failure compared to other GLP-1 receptor agonists. When used as a monotherapy for diabetes or in combination with other hypoglycemic agents, it can reduce HbA1c by up to 1%, which is lower than several GLP-1 receptor agonists. It has little benefit in terms of weight loss compared to other GLP-1 receptor agonists. There is a concern that there is an imbalance in the number of pancreatitis cases in the approved program and that injection site reactions have led to up to 2% of subjects discontinuing treatment. A large, long-term study is underway to determine whether abiglutide, which has low gastrointestinal intolerance, is suitable for treating patients at increased risk of cardiovascular events. [1]

C148H224N40O45

3283.6

3281.646

782500-75-8

Albiglutide fragment TFA; Albiglutide fragment; 224638-84-0

145994868

H-His-Gly-Glu-Gly-aThr-Phe-aThr-Ser-Asp-Val-Ser-Ser-Tyr-Leu-Glu-Gly-Gln-D-Ala-D-Ala-Lys-Glu-Phe-aIle-D-Ala-Trp-Leu-Val-Lys-Gly-Arg-NH2; L-histidyl-glycyl-L-alpha-glutamyl-glycyl-L-allothreonyl-L-phenylalanyl-L-allothreonyl-L-seryl-L-alpha-aspartyl-L-valyl-L-seryl-L-seryl-L-tyrosyl-L-leucyl-L-alpha-glutamyl-glycyl-L-glutaminyl-D-alanyl-D-alanyl-L-lysyl-L-alpha-glutamyl-L-phenylalanyl-L-alloisoleucyl-D-alanyl-L-tryptophyl-L-leucyl-L-valyl-L-lysyl-glycyl-L-argininamide

HGEGXFXSDVSSYLEGQAAKEFXAWLVKGR

White to yellow powder

1.5±0.1 g/cm3

1.661

-5.2

49

50

109

233

7620

29

O=C([C@H](CC(C)C)NC([C@H](CC1=CNC2C=CC=CC1=2)NC([C@@H](C)NC([C@H]([C@H](C)CC)NC([C@H](CC1C=CC=CC=1)NC([C@H](CCC(=O)O)NC([C@H](CCCCN)NC([C@@H](C)NC([C@@H](C)NC([C@H](CCC(N)=O)NC(CNC([C@H](CCC(=O)O)NC([C@H](CC(C)C)NC([C@H](CC1C=CC(=CC=1)O)NC([C@H](CO)NC([C@H](CO)NC([C@H](C(C)C)NC([C@H](CC(=O)O)NC([C@H](CO)NC([C@H]([C@H](C)O)NC([C@H](CC1C=CC=CC=1)NC([C@@H]([C@H](C)O)NC(CNC([C@H](CCC(=O)O)NC(CNC([C@H](CC1=CN=CN1)N)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)N[C@H](C(N[C@H](C(NCC(N[C@H](C(N)=O)CCCNC(=N)N)=O)=O)CCCCN)=O)C(C)C

JYDZPPZAYQTOIV-OTSUTHPESA-N

InChI=1S/C148H224N40O45/c1-16-76(10)119(145(231)166-79(13)125(211)174-103(59-85-62-158-90-35-24-23-34-88(85)90)135(221)176-99(55-73(4)5)136(222)185-117(74(6)7)143(229)173-92(36-25-27-51-149)127(213)160-65-109(196)167-91(122(153)208)38-29-53-157-148(154)155)187-137(223)101(56-82-30-19-17-20-31-82)177-132(218)97(46-50-115(204)205)172-131(217)93(37-26-28-52-150)170-124(210)78(12)164-123(209)77(11)165-130(216)96(43-47-108(152)195)169-111(198)66-161-129(215)95(45-49-114(202)203)171-133(219)98(54-72(2)3)175-134(220)100(58-84-39-41-87(194)42-40-84)178-140(226)105(68-189)181-142(228)107(70-191)182-144(230)118(75(8)9)186-139(225)104(61-116(206)207)179-141(227)106(69-190)183-147(233)121(81(15)193)188-138(224)102(57-83-32-21-18-22-33-83)180-146(232)120(80(14)192)184-112(199)67-162-128(214)94(44-48-113(200)201)168-110(197)64-159-126(212)89(151)60-86-63-156-71-163-86/h17-24,30-35,39-42,62-63,71-81,89,91-107,117-121,158,189-194H,16,25-29,36-38,43-61,64-70,149-151H2,1-15H3,(H2,152,195)(H2,153,208)(H,156,163)(H,159,212)(H,160,213)(H,161,215)(H,162,214)(H,164,209)(H,165,216)(H,166,231)(H,167,196)(H,168,197)(H,169,198)(H,170,210)(H,171,219)(H,172,217)(H,173,229)(H,174,211)(H,175,220)(H,176,221)(H,177,218)(H,178,226)(H,179,227)(H,180,232)(H,181,228)(H,182,230)(H,183,233)(H,184,199)(H,185,222)(H,186,225)(H,187,223)(H,188,224)(H,200,201)(H,202,203)(H,204,205)(H,206,207)(H4,154,155,157)/t76-,77-,78-,79-,80+,81+,89+,91+,92+,93+,94+,95+,96+,97+,98+,99+,100+,101+,102+,103+,104+,105+,106+,107+,117+,118+,119+,120+,121+/m1/s1

(4S)-5-[[2-[[(2S,3S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-5-amino-1-[[(2R)-1-[[(2R)-1-[[(2S)-6-amino-1-[[(2S)-1-[[(2S)-1-[[(2S,3R)-1-[[(2R)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[2-[[(2S)-1-amino-5-carbamimidamido-1-oxopentan-2-yl]amino]-2-oxoethyl]amino]-1-oxohexan-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]-1-oxohexan-2-yl]amino]-1-oxopropan-2-yl]amino]-1-oxopropan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-2-oxoethyl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(4-hydroxyphenyl)-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-3-carboxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-3-hydroxy-1-oxobutan-2-yl]amino]-2-oxoethyl]amino]-4-[[2-[[(2S)-2-amino-3-(1H-imidazol-5-yl)propanoyl]amino]acetyl]amino]-5-oxopentanoic acid

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)

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.

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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.)