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Liraglutide Suppliers list
Company Name: Rixing Chemical CO.,LTD
Tel: 13237129059
Products Intro: Product Name:Liraglutide
Purity:98% Package:1gram/bottle;10g/bottle;100g/bottle;1kg/foilbag
Company Name: Shenzhen Sendi Biotechnology Co.Ltd.
Tel: 0755-23311925 18102838259
Products Intro: Product Name:Liraglutide
Purity:99% Package:15400/G
Company Name: Henan DaKen Chemical CO.,LTD.
Tel: +86-371-55531817
Products Intro: Product Name:Liraglutide
Purity:99% Package:100g,500g,1KG,10KG,100KG
Company Name: Beijing Cooperate Pharmaceutical Co.,Ltd.
Tel: +86-10-60279497 +86(0)15646567669
Products Intro: Product Name:Liraglutide
Purity:98% Package:100G;1KG;50KG;100KG;1000KG
Company Name: Henan Tianfu Chemical Co.,Ltd.
Tel: 0371-55170693
Products Intro: CAS:204656-20-2
Purity:99% Package:500G;1KG;5KG;25KG

Lastest Price from Liraglutide manufacturers

  • Liraglutide
  • US $8.00 / G
  • 2018-07-25
  • CAS:204656-20-2
  • Min. Order: 1G
  • Purity: 99%
  • Supply Ability: 20kg
Liraglutide Basic information
Overview Pharmacodynamic and pharmacology properties Pharmacokinetics properties Dosage and administration Tolerability References
Product Name:Liraglutide
Synonyms:Liraglutide;Glycine, L-histidyl-L-alanyl-L-alpha-glutamylglycyl-L-threonyl-L-phenylalanyl-L-threonyl-L-seryl-L-alpha-aspartyl-L-valyl-L-seryl-L-seryl-L-tyrosyl-L-leucyl-L-alpha-glutamylglycyl-L-glutaminyl-L-alanyl-L-alanyl-N6-(N-(1-oxohexadecyl)-L-gamma-glutamyl)-L-lysyl-L-alpha-glutamyl-L-phenylalanyl-L-isoleucyl-L-alanyl-L-tryptophyl-L-leucyl-L-valyl-L-arginylglycyl-L-arginyl-;Liraglutida;Liraglutida [inn-spanish];Liraglutide [usan:inn];Liraglutidum;Liraglutidum [inn-latin];N26-(Hexadecanoyl-gamma-glutamyle)-(34-arginine)glp-1-(7-37)-peptide
Product Categories:GLP
Mol File:204656-20-2.mol
Liraglutide Structure
Liraglutide Chemical Properties
Safety Information
MSDS Information
Liraglutide Usage And Synthesis
OverviewType 2-diabetes mellitus(T2DM) is a progressive disease associated with significant morbidity and mortality. Glucagon like peptide-1(GLP-1) is an incretin hormone secreted from the small intestine that lowers fasting and postprandial glucose through multiple mechanisms including glucose-dependent insulin secretion, reduction of glucagon secretion, delaying gastric emptying and increased satiety[1-4]. Liraglutide, a human glucagon-like peptide 1(GLP-1) analogue is a treatment for T2DM that is administered as a once-daily subcutaneous injection. Liraglutide is a GLP-1 analog in which lysine at position 34 has been replaced with arginine, and palmitic acid has been attached via glutamoyl spacer to lysine at position 26[1-4]. No animal-derived raw materials or excipients are used in the production of liraglutide. The drug product is a solution for subcutaneous injection containing 6.0 mg/ml of the drug substance presented in a pre-filled, multi-dose pen-injector. Unlike GLP-1, liraglutide has a pharmacokinetic and pharmacodynamic profile in human suitable for once daily administration. Following subcutaneous administration, the protracted action profile is based on three mechanisms: self-association, which results in slow absorption, binding to albumin and stability toward the DPP-4 enzyme both resulting in a prolonged plasma half-life. The analog is produced as the polypeptide precursor by r-DNA technology with Saccharomyces cerevisiae strain YES2085 as the production strain. The peptide is acylated with a fatty acid chain during down-stream processing[1-4].

Figure 1 the chemical structure of Liraglutide
Liraglutide is a long-acting GLP-1 analog, designed to bind to albumin as the main molecular mechanism of protraction[1-4]. In vitro, this was shown in the receptor cAMP as well as binding assay where addition of albumin shifted the dose-response and/or binding curve to the right. The apparent reduced potency of liraglutide underlines that only the free fraction of liraglutide is responsible for its pharmacological effect in vitro as well as in vivo. Furthermore, liraglutide in a pharmaceutical solution forms a micell-like heptamer that may contribute to the slow absorption from the subcutis[1-4]. Liraglutide is a potent, selective and efficacious agonist on the human as well as mouse, rat, rabbit, pig and Cynomolgus monkey GLP-1 receptor. Liraglutide has been shown to exert a number of actions in vitro that are known to be specific GLP-1 effects[1-4]. Liraglutide has also been shown stimulate insulin secretion from isolated β-cell islets in a glucose-dependent manner in vitro. Liraglutide-attenuated β-cell apoptosis in vitro under adverse conditions with high concentrations of free fatty acids and proinflammatory cytokines. Moreover, a proliferative effect on primary rat β-cells was demonstrated for liraglutide in vitro whereas no consistent effect was observed under hyperglycemic conditions in vivo[1-4].
Pharmacodynamic and pharmacology propertiesLiraglutide is an acylated GLP-1 analogue that shares 97 % amino acid sequence homology to human endogenous GLP-1 (7–37)[1–4]. The single amino acid substitution of lysine with arginine at position 34 and the attachment of a C16 fatty acid chain to lysine at position 26 enables liraglutide to self-associate and form a heptameric structure, which delays absorption from the subcutaneous injection site and provides protection against degradation by DPP-4 enzyme and neutral endopeptidases. As a consequence, liraglutide has a much longer half-life than endogenous GLP-1 (&13 h vs. 1.5–2 min)[1–4].
Liraglutide binds to and activates the GLP-1 receptor, which is a membrane bound cell-surface receptor coupled to adenyl cyclase by the stimulatory G-protein (Gs) in pancreatic b cells (but not in pancreatic a-cells) and is the target for endogenous GLP-1[1, 2]. This results in increased intracellular cyclic monophosphate and subsequent liraglutide dose-dependent insulin release in patients with elevated glucose levels. At the same time, liraglutide acts in a glucose-dependent manner to decrease inappropriately high glucagon secretion, thereby blocking the effects of glucagon on hepatic glucose output. In the presence of liraglutide, as blood glucose concentrations decrease, the secretion of insulin diminishes and blood glucose concentrations approach euglycaemia[1, 2]. In addition to these glucoregulatory mechanisms of action in patients with type 2 diabetes, liraglutide slightly delays gastric emptying, and reduces bodyweight and body fat mass by reducing hunger and lowering energy intake; these effects may contribute to the beneficial effects of liraglutide in patients with type 2-diabetes[1, 2, 5, 6]. As reviewed previously[1, 2], in patients with type 2 diabetes and/or in preclinical studies, liraglutide dosedependently reduced glycated haemoglobin (HbA1c), fasting plasma glucose (FPG) and postprandial plasma glucose levels, with sustained improvements in glucose levels over a 24-h dosage interval. In addition, liraglutide increased insulin secretion, reduced postprandial glucagon secretion, improved surrogate measures of b-cell function, reduced systolic blood pressure (SBP) and improved some biomarkers of cardiovascular (CV) risk in patients with type 2 diabetes[1, 2], including suppression of postprandial triglyceride and apolipoprotein B48 levels after a fat-rich meal[7]. Improvements in glycaemic control and other efficacy outcomes in adult patients with type 2 diabetes receiving liraglutide monotherapy or add-on therapies to other antidiabetic drugs in large phase III trials.
Pharmacokinetics propertiesThe pharmacokinetic profile of subcutaneous liraglutide did not differ to a clinically meaningful extent when different injection sites were used (upper arm, abdomen and thigh)[3]. Following subcutaneous administration, liraglutide was slowly absorbed, with maximum plasma concentrations (Cmax) attained after 8–12h[3, 4]. Liraglutide showed dose-proportional absorption across the therapeutic dose range of 0.6–1.8 mg[3, 4]. Mean Cmax and total exposure of liraglutide after a single 0.6 mg dose were 35 ng/mL and 960 ng??h/mL, respectively[3]. After a 1.8 mg dose, the average steady-state concentration of liraglutide over a 24-h period was 128 ng/mL[3]. Following subcutaneous administration, the mean apparent volume of distribution of liraglutide was 11–17 L[4]. The mean volume of distribution after intravenous administration was 0.07 L/kg[3, 4]. The absolute bioavailability of liraglutide following subcutaneous administration is approximately 55 %. Liraglutide is extensively bound to plasma protein following subcutaneous administration (98 %)[3, 4].
Liraglutide is metabolized in a manner similar to that of large proteins, with no specific organ identified as a major route of elimination[3, 4]. During the 24-h period following administration of a single radiolabelled dose of liraglutide to healthy volunteers, the major component in plasma was unchanged drug, with two minor plasma metabolites detected (B9 and B5 % of total plasma radioactivity exposure). No parent drug was detected in the faeces and urine. A minor portion of the radiolabelled dose was detected as liraglutide-related metabolites in the faeces (5 %) and urine (6 %) during the first 6–8 days after administration. The mean clearance following a single subcutaneous dose of liraglutide was approximately 1.2 L/ h and the mean elimination half-life was approximately 13 h, allowing for once-daily administration[3, 4].
Dosage and administrationSubcutaneous liraglutide is approved in several countries for the treatment of patients with type 2 diabetes, including in the USA[3] and Europe[4]. In the USA, subcutaneous liraglutide is indicated in patients with type 2 diabetes as an adjunct to the diet and exercise to improve glycaemic control[3]. In the EU, it is indicated for the treatment of adults with type 2 diabetes to achieve glycaemic control in combination with OADs and/or basal insulin when these, together with diet and exercise, do not provide adequate glycaemic control[4]. Liraglutide is not recommended as first-line therapy in patients with inadequate glycaemic control on diet and exercise[3].
Liraglutide is administered subcutaneously once daily at any time of the day, without regard to food[3, 4]. The initial starting dosage is 0.6 mg/day for 1 week; this low initial dosage is intended to reduce the risk of GI adverse events and is not effective for glycaemic control. After 1[3] or C1[4] week, the dosage of liraglutide should be increased to 1.2 mg/day and, thereafter, if the 1.2 mg/day doesn’t provide effective glycaemic control the dosage may be increased to 1.8 mg/day. If the drug is added to metformin alone or in combination with a thiazolidinedione, the dosages of these coadministered drugs may be continued unchanged. When initiating liraglutide treatment, consider reducing the dosage of concomitantly administered insulin secretagogues (such as sulfonylureas) or basal insulin to reduce the risk of hypoglycaemia [3, 4]. Although self-monitoring of glucose levels is not necessary for liraglutide, it should be considered when initiating liraglutide therapy in patients receiving concomitant sulfonylurea or basal insulin therapy to reduce the risk of hypoglycaemia[4]. No dosage adjustment is required in elderly patients (aged 65 years)[3, 4]. The efficacy of liraglutide in children and adolescents >18 years of age has not been established[3, 4]; in the USA, liraglutide is not recommended in paediatric patients[4]. In the EU, no dosage adjustment is required in patients with mild renal impairment (CLCR 60–90 mL/min) and there is very limited experience in those moderate or severe renal impairment; thus, liraglutide can currently not be recommended in these patients or in those with ESRD[4]. In the USA, it is recommended that liraglutide should be used with caution in patients with renal impairment, including those with ESRD, since there have been postmarketing reports of acute renal failure and worsening of chronic renal failure during liraglutide treatment[3]. No dosage adjustments are required in patients with renal impairment[3].
TolerabilitySubcutaneous liraglutide, as monotherapy or add-on therapy to antidiabetic drugs, was generally well tolerated in clinical trials and extension studies (B2 years’ treatment). Based on a pooled analysis of five double-blind trials (C26 weeks’ duration), 7.8 % of liraglutide recipients discontinued treatment because of adverse events compared with 3.4 % of patients in the comparator groups[3]. Nausea (2.8 % in liraglutide groups vs. 0 % in comparator groups) and vomiting (1.5 vs. 0.1 %) were the most common adverse reactions leading to treatment withdrawal, with most patients withdrawing within the first 2–3 months of liraglutide therapy. Most treatment-emergent adverse events occurring during liraglutide therapy were gastrointestinal (GI) in nature, of mild or moderate intensity and resolved after the first few weeks of treatment[3]. Injection site reactions (e.g. rash and erythema) occurred in approximately 2 % of patients participating in five double-blind trials (C26 weeks’ duration), with 0.2 % of patients discontinuing treatment because of these events[4].
In postmarketing surveillance studies there have been reports of acute pancreatitis, including fatal and non-fatal haemorrhagic or necrotizing pancreatitis, in patients treated with liraglutide[3, 4]. In clinical trials, 13 liraglutide recipients and one glimepiride recipient experienced pancreatitis (2.7 vs. 0.5 cases/1,000 patient-years) [3]. Of the 13 liraglutide-treated recipients, nine patients had acute pancreatitis and four had chronic pancreatitis, with some of the 13 patients having other risk factors for pancreatitis, such as a history of cholelithiasis or alcohol abuse. Although clinical causality could not be established, one of the 13-liraglutide recipients had pancreatitis with necrosis that led to death[3].
In clinical trials, seven cases of papillary thyroid carcinoma were reported in liraglutide-treated patients compared one case in a comparator group (1.5 vs. 0.5 cases/ 1,000 patient-years)[3]. Most of these papillary thyroid carcinomas were <1 cm in greatest diameter and were diagnosed in surgical pathology specimens after thyroidectomy prompted by results from protocol-specified screening procedures[3].
  1. Perry CM. Liraglutide: a review of its use in the management of type 2 diabetes mellitus. Drugs. 2011;71(17):2347–73.
  2. Croom KF, McCormack PL. Liraglutide: a review of its use in type 2 diabetes mellitus. Drugs. 2009;69(14):1985–2004.
  3. Novo Nordisk A/S. Victoza liraglutide (rDNA origin) injection: US prescribing information. 2013. victoza.pdf. Accessed 20 Aug 2014.
  4. Novo Nordisk A/S. Victoza: EU summary of product characteristics. 2014. library/EPAR_-_Product_Information/human/001026/WC5000500 17.pdf. Accessed 20 Aug 2014.
  5. Flint A, Kapitza C, Zdravkovic M. The once-daily human GLP-1 analogue liraglutide impacts appetite and energy intake in patients with type 2 diabetes after short-term treatment. Diabetes Obes Metab. 2013;15(10):958–62.
  6. Horowitz M, Flint A, Jones KL, et al. Effect of the once-daily human GLP-1 analogue liraglutide on appetite, energy intake, energy expenditure and gastric emptying in type 2 diabetes. Diabetes Res Clin Pract. 2012; 97(2):258–66.
  7. Hermansen K, Baekdal TA, During M, et al. Liraglutide suppresses postprandial triglyceride and apolipoprotein B48 elevations after a fat-rich meal in patients with type 2 diabetes: a randomized, double-blind, placebo-controlled, cross-over trial. Diabetes Obes Metab. 2013;15(11):1040–8.
DefinitionChEBI: A lipopeptide that is an analogue of human GLP-1 in which the lysine residue at position 27 is replaced by arginine and a hexadecanoyl group attached to the remaining lysine via a glutamic acid spacer. Used as an adjunct to diet and exercise to improve gly emic control in adults with type 2 diabetes mellitus.
Liraglutide Preparation Products And Raw materials
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