GLP-1 receptor

Compared to liraglutide and albiglutide, which are long-acting GLP-1-based peptides, lixisenatide is a short-acting GLP-1-receptor agonist with a half-life of 2-4 hours. Insulin release that is stimulated by glucose can be markedly enhanced by lixisenatide. When administered subcutaneously, lixisenatide reduces plasma glucose levels in healthy normoglycemic dogs in a dose-dependent manner following an oral glucose challenge. It also significantly lowers postprandial glucose excursions, as evidenced by a 67% reduction when compared to a placebo, without contributing to an increase in insulin concentrations. Lixisenatide's impact on dogs' postprandial blood glucose excursions is thought to be partly caused by delayed intestinal glucose absorption and inhibition of stomach emptying. In the db/db mouse and ZDF rat, dose-dependent decreases in plasma glucose following an oral glucose challenge have also been shown. Crucially, at physiological glucose concentrations, this activity is insensitive to glucose and is glucose-dependent. Chronic lixisenatide administration in db/db mice is associated with significant dose-dependent reductions in glycosylated hemoglobin (HbA1c) and prevents the progressive deterioration in glucose tolerance observed in control animals. For a duration of 12 weeks, lixisenatide 50 μg/kg/day subcutaneous infusion significantly lowers basal blood glucose and enhances oral glucose tolerance in ZDF rats when compared to control animals. In rats with normoglycemia, it has no hypoglycemic effect and has no effect on HbA1c. By promoting islet cell proliferation and neogenesis and inhibiting islet cell apoptosis, lixisenatide can preserve beta cell mass and function[1]. In diabetic animals, lixisenatide maintains pancreatic responsiveness[3].

Lixisenatide, shown in in vitro receptor binding studies, is a short-acting agonist of the glucagon-like peptide-1 receptor (GLP-1R), with an IC50 value of 1.4 nM for the human GLP-1 receptor. Receptor binding studies demonstrated that the affinity of Lixisenatide/ZP10A for the human GLP-1 receptor was 4-fold greater than the affinity of GLP-1 (7-36) amide.

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GLP-1 Receptor Binding Studies. [2]
In short, CHO-K1 cells harboring the human recombinant GLP-1 receptor were harvested. The membrane fraction containing the receptor was purified and used for... Binding of ZP10A to Human GLP-1 Receptor. The concentration resulting in half-maximal inhibition (IC50) of binding to the human GLP-1 receptor expressed in CHO-K1 cells was 5.5 ± 1.3 nM for GLP-1 (7-36) amide, a value within the range of those reported for GLP-1 binding to the endogenous receptor found in islet cell lines and to the recombinant receptor expressed in COS-7 cells (Goke and Conlon, 1988; Goke et al., 1989; Fehmann and Habener, 1991; Thorens, 1992; Wheeler et al., 1993). The IC50...

Lixisenatide has the ability to prevent apoptosis caused by lipids and cytokines in Ins-1 cells, a β-cell line derived from rats. More significantly, lixisenatide can maintain insulin synthesis, storage, and pancreatic β-cell function in vitro and prevent lipotoxicity-induced insulin depletion in human islets.

Pphosphate-buffered saline, pH 7.4; 0.01, 0.1, 1, 10, and 100 nmol/kg; i.p.
Male db/db mice C57BLKS/J-Leprdb/Leprdb

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ZP10A demonstrated dose-dependent improvement of glucose tolerance with an ED50 value of 0.02 nmol/kg i.p. in an oral glucose tolerance test (OGTT) in diabetic db/db mice. After 42 days of treatment, ZP10A dose-dependently (0, 1, 10, or 100 nmol/kg b.i.d.; n = 10/group), decreased glycosylated hemoglobin (HbA1C) from 8.4 +/- 0.4% (vehicle) to a minimum of 6.2 +/- 0.3% (100 nmol/kg b.i.d.; p < 0.05 versus vehicle) in db/db mice. Fasting blood glucose (FBG), glucose tolerance after an OGTT, and HbA1C levels were significantly improved in mice treated with ZP10A for 90 days compared with vehicle-treated controls. Interestingly, these effects were preserved 40 days after drug cessation in db/db mice treated with ZP10A only during the first 50 days of the study. Real-time polymerase chain reaction measurements demonstrated that the antidiabetic effect of early therapy with ZP10A was associated with an increased pancreatic insulin mRNA expression relative to vehicle-treated mice. In conclusion, long-term treatment of diabetic db/db mice with ZP10A resulted in a dose-dependent improvement of FBG, glucose tolerance, and blood glucose control. Our data suggest that ZP10A preserves beta-cell function. ZP10A is considered one of the most promising new drug candidates for preventive and therapeutic intervention in type 2 diabetes.[2]

Absorption, Distribution and Excretion
Following subcutaneous injection, the median time to peak concentration (Tmax) of lixilamide is 1–3.5 hours, with no clinically significant difference in absorption rate among different injection sites (e.g., thigh, abdomen, or arm). Lixilamide may be cleared via glomerular filtration and proteolytic degradation. The apparent volume of distribution after subcutaneous injection is approximately 100 liters. The mean apparent clearance of lixilamide is approximately 35 liters/hour. Metabolisms/Metabolites Lixilamide may be metabolized via nonspecific proteolytic degradation. Biological Half-Life Following multiple doses in patients with type 2 diabetes, the mean terminal half-life of lixilamide is approximately 3 hours.

Hepatotoxicity
In large clinical trials, the incidence of elevated serum enzymes in the lixilamide treatment group was not higher than in the placebo or control groups. In a pooled safety analysis of over 5000 patients, 0.6% of patients in both the lixilamide and placebo groups experienced ALT elevations exceeding three times the upper limit of normal, and no treatment-related clinically significant liver injury was reported. Since lixilamide's approval, no published cases of lixilamide-induced hepatotoxicity have been reported, and liver injury is not listed as an adverse event in the product information leaflet. Therefore, as with other GLP-1 analogs, liver injury caused by lixilamide, even if it occurs, is certainly very rare. Probability Score: E (Unlikely to be the cause of clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation Currently, there is no information regarding the clinical use of lixilamide during lactation. Because lixilamide is a large peptide molecule with a molecular weight of 4858 Daltons, its content in breast milk is likely to be very low, and it is unlikely to be absorbed as it is likely to be destroyed in the infant's gastrointestinal tract. Until more data are available, breastfeeding women should use lixilamide with caution, especially when breastfeeding newborns or premature infants.
◉ Effects on breastfed infants
As of the revision date, no relevant published information was found.
◉ Effects on lactation and breast milk
As of the revision date, no relevant published information was found.

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Protein binding
Lixilamide binds to human plasma proteins at a rate of approximately 55%.

[1]. Core Evid. 2011:6:67-79.

[2]. J Pharmacol Exp Ther. 2003 Nov;307(2):490-6.

[3]. Regul Pept. 2010 Sep 24;164(2-3):58-64.

[4]. Diabetes Ther. 2016 Jun 18.

[5]. Regul Pept. 2013 Aug 10;185:1-8.

Lixisenatide is a 44-membered polypeptide consisting of the following residues linked in sequence: L-His, Gly, L-Glu, Gly, L-Thr, L-Phe, L-Thr, L-Ser, L-Asp, L-Leu, L-Ser, L-Lys, L-Gln, L-Met, L-Glu, L-Glu, L-Glu, L-Ala, L-Val, L-Arg, L-Leu, L-Phe, L-Ile, L-Glu, L-Trp, L-Leu, L-Lys, L-Asn, Gly, Gly, LPro, L-Ser, L-Ser, Gly, L-Ala, L-Pro, L-Pro, L-Ser, L-Lys, L-Lys, L-Lys, L-Lys, L-Lys and L-Lys-NH2. Lixilate is a glucagon-like peptide-1 (GLP-1) receptor agonist used to treat type 2 diabetes in adults. It is a glucagon-like peptide-1 receptor agonist, hypoglycemic agent, and neuroprotective agent. It is a polypeptide and peptide amide. Lixilate is manufactured by Sanofi-Aventis and marketed in the United States as Adlyxin and in the European Union as Lyxumia. Adlyxin was approved by the U.S. Food and Drug Administration (FDA) on July 28, 2016. Lixilate is a recombinant DNA-produced polypeptide, an analog of human glucagon-like peptide-1 (GLP-1), which can be used alone or in combination with other antidiabetic drugs, in conjunction with diet and exercise, to treat type 2 diabetes. Lixilate treatment is not associated with elevated serum enzymes or clinically significant liver injury events.
See also: Insulin glargine; Lixilate (ingredients). Drug Indications Lixilate is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes. It can also be used in combination with insulin glargine for the same indication. Lixilate is indicated for the treatment of type 2 diabetes in adults when oral hypoglycemic agents and/or basal insulin combined with diet and exercise fail to provide adequate glycemic control. Mechanism of Action Lixilate activates the GLP-1 receptor, thereby activating adenylate cyclase. This increases the intracellular concentration of cyclic adenosine monophosphate (cAMP), which in turn activates protein kinase A (PKA), as well as Epac1 and Epac2. PKA, Epac1, and Epac2 are involved in the release of Ca2+ from the endoplasmic reticulum, a process known as the "amplification" pathway. When this pathway is activated, it increases insulin release. Lixilate increases glucose-stimulated insulin secretion by activating this amplification pathway. Lixilate is a once-daily glucagon-like peptide-1 (GLP-1) receptor agonist that mimics many of the beneficial effects of endogenous GLP-1, thereby improving glycemic control with minimal hypoglycemia and weight loss. A Phase II clinical trial demonstrated that once-daily 20 μg lixilate restored first-phase insulin release and improved second-phase insulin response in patients with type 2 diabetes. Once- or twice-daily administration for 4 weeks significantly reduced postprandial and fasting blood glucose levels as well as glycated hemoglobin (HbA1c). Currently, the GETGOAL Phase III clinical trial is evaluating the efficacy and safety of once-daily lixilate. Results showed that compared to placebo in combination with commonly used hypoglycemic agents, lixilate had a beneficial effect on HbA1c without increasing the risk of hypoglycemia and contributed to weight loss. Adverse reactions are similar to those of marketed GLP-1 receptor agonists, with gastrointestinal reactions being the most common. Preclinical studies have confirmed that both GLP-1 receptor agonists and long-acting insulin analogs have protective effects on β-cells. The significant effect of lixilamide on postprandial blood glucose, and its combined use with long-acting basal insulin analogs, provides a theoretical basis for further improving glycemic control. It is hoped that this combination therapy will enhance glycemic control and may benefit pancreatic islet cells, thus providing a new approach to glycemic control for patients with type 2 diabetes and preventing long-term complications. [1]

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Glucagon-like peptide-1 (GLP-1) receptor is an established therapeutic target for type 2 diabetes (T2DM). Drugs that activate this receptor can improve glucose tolerance, reduce the risk of hypoglycemia, and potentially delay disease progression. Lixilamide is a novel, potent, and selective GLP-1 receptor agonist currently under development. Preclinical pharmacological profiles of lixilamide suggest that its mechanism of action is closely related to long-term maintenance of glycemic homeostasis. Lixilamide can protect Ins-1 cells (a rat-derived β-cell line) from lipid- and cytokine-induced apoptosis. More importantly, lixilamide can prevent lipotoxicity-induced insulin depletion in human pancreas and maintain insulin production, storage, and pancreatic β-cell function in vitro. In animal models of type 2 diabetes, lixilamide has also been shown to enhance insulin biosynthesis and increase pancreatic β-cell volume. The effect of lixilamide on glucose-stimulated insulin secretion is strictly dependent on glucose. In diabetic animal models, lixilamide has a rapid onset and long duration of action, improving basal blood glucose and glycated hemoglobin (HbA1c) levels and preventing the deterioration of pancreatic responsiveness and glucose homeostasis. Lixilamide can also delay gastric emptying and reduce food intake. Currently, a large-scale phase III clinical trial is underway to further evaluate the efficacy and safety of lixilamide. This article reviews the preclinical pharmacological characteristics of lixilamide. [3]

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Introduction: It is unclear to what extent a decrease in postprandial glucagon can reduce postprandial blood glucose in patients with type 2 diabetes (T2DM). This analysis aimed to determine whether the reduction in postprandial glucagon after treatment with the glucagon-like peptide-1 receptor agonist lixilamide was associated with a decrease in postprandial blood glucose and glycated hemoglobin (HbA1c) in patients with type 2 diabetes mellitus (T2DM). Methods: A post-hoc analysis was performed on pooled data from modified intention-to-treat populations of two phase 3 lixilamide clinical trials (GetGoal-M (lixilamide plus placebo plus metformin) and GetGoal-S (lixilamide plus placebo plus sulfonylureas [SU] ± metformin)). Standardized postprandial trials were performed at baseline and week 24, and glucagon levels were assessed 2 hours postprandial, and their correlation with changes in postprandial blood glucose and HbA1c at 2 hours was analyzed. Results: Compared with the placebo group, the lixilamide group showed a significant reduction in postprandial 2-hour glucagon levels at week 24 (P < 0.00001). The mean change in postprandial glucagon was significantly associated with a decrease in postprandial blood glucose (P < 0.00001) and HbA1c (P < 0.00001). Conclusion: In patients with type 2 diabetes whose blood glucose is poorly controlled by metformin and/or sulfonylureas, the decrease in postprandial glucagon levels after lixilate treatment was associated with a decrease in postprandial blood glucose and HbA1c. This suggests that a decrease in postprandial glucagon levels helps lixilate improve overall glycemic control. [4] Objective: To determine the effects of lixilate (a novel once-daily glucagon-like peptide-1 receptor agonist) on postprandial blood glucose (PPG) and gastric emptying, and the relationship between these effects in patients with type 2 diabetes (T2DM). Methods: Data were obtained from a randomized, double-blind, placebo-controlled, parallel-group study lasting 28 days in patients with T2DM who were receiving ≤2 oral hypoglycemic agents. Lixilate was administered subcutaneously at doses ranging from 5 to 20 μg, increasing by 2.5 μg every 5 days. Blood glucose was measured before and after three standard meals (breakfast, lunch, and dinner). Gastric emptying after a standardized breakfast was measured using a 13C-octanoic acid breath test at baseline (day -1) and on day 28. Results: 21 and 22 patients were randomly assigned to the lixilate 20 μg once-daily group and the placebo group, respectively. Compared with the placebo group, the lixilate 20 μg once-daily group showed reduced postprandial blood glucose (PPG) after breakfast (p<0.0001), lunch (p<0.001), and dinner (p<0.05). Therefore, taking 20 μg of lixilate in the morning can have a pharmacodynamic effect on blood glucose throughout the day. Compared with baseline, once-daily administration of 20 μg lixilamide significantly prolonged gastric emptying time (50% of emptying time), while no such phenomenon was observed in the placebo group (change ± standard deviation from baseline: -24.1 ± 133.1 minutes in the placebo group and 211.5 ± 278.5 minutes in the lixilamide group; p < 0.01). Once-daily administration of 20 μg lixilamide showed a negative correlation between the area under the blood glucose curve after breakfast and gastric emptying time (n = 17, r² = 0.51, p < 0.05), while no such correlation was observed in the placebo group. Conclusion: This study suggests that once-daily administration of 20 μg lixilamide can reduce postprandial blood glucose fluctuations in patients with type 2 diabetes, which may be due to the sustained slowing of gastric emptying. [5]

C215H347N61O65S

4858.4904282093

4857.551

C, 53.15; H, 7.20; N, 17.59; O, 21.40; S, 0.66

1997361-87-1

Lixisenatide; 320367-13-3

16139342

H-His-Gly-Glu-Gly-Thr-Phe-Thr-Ser-Asp-Leu-Ser-Lys-Gln-Met-Glu-Glu-Glu-Ala-Val-Arg-Leu-Phe-Ile-Glu-Trp-Leu-Lys-Asn-Gly-Gly-Pro-Ser-Ser-Gly-Ala-Pro-Pro-Ser-Lys-Lys-Lys-Lys-Lys-Lys-NH2; L-histidyl-glycyl-L-alpha-glutamyl-glycyl-L-threonyl-L-phenylalanyl-L-threonyl-L-seryl-L-alpha-aspartyl-L-leucyl-L-seryl-L-lysyl-L-glutaminyl-L-methionyl-L-alpha-glutamyl-L-alpha-glutamyl-L-alpha-glutamyl-L-alanyl-L-valyl-L-arginyl-L-leucyl-L-phenylalanyl-L-isoleucyl-L-alpha-glutamyl-L-tryptophyl-L-leucyl-L-lysyl-L-asparagyl-glycyl-glycyl-L-prolyl-L-seryl-L-seryl-glycyl-L-alanyl-L-prolyl-L-prolyl-L-seryl-L-lysyl-L-lysyl-L-lysyl-L-lysyl-L-lysyl-L-lysinamide

HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPSKKKKKK; H-HGEGTFTSDLSKQMEEEAVRLFIEWLKNGGPSSGAPPSKKKKKK-[NH2]

White to off-white solid powder

-30.8

70

77

170

342

11800

42

S(C)CC[C@@H](C(N[C@@H](CCC(=O)O)C(N[C@@H](CCC(=O)O)C(N[C@@H](CCC(=O)O)C(N[C@@H](C)C(N[C@H](C(N[C@@H](CCCNC(=N)N)C(N[C@H](C(N[C@@H](CC1C=CC=CC=1)C(N[C@H](C(N[C@@H](CCC(=O)O)C(N[C@@H](CC1=CNC2C=CC=CC1=2)C(N[C@@H](CC(C)C)C(N[C@@H](CCCCN)C(N[C@@H](CC(N)=O)C(NCC(NCC(N1CCC[C@H]1C(N[C@@H](CO)C(N[C@@H](CO)C(NCC(N[C@@H](C)C(N1CCC[C@H]1C(N1CCC[C@H]1C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N[C@H](C(N)=O)CCCCN)=O)CCCCN)=O)CCCCN)=O)CCCCN)=O)CCCCN)=O)CCCCN)=O)CO)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)=O)[C@@H](C)CC)=O)=O)CC(C)C)=O)=O)C(C)C)=O)=O)=O)=O)=O)NC([C@H](CCC(N)=O)NC([C@H](CCCCN)NC([C@H](CO)NC([C@H](CC(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

XVVOERDUTLJJHN-IAEQDCLQSA-N

InChI=1S/C215H347N61O65S/c1-16-115(10)173(210(337)256-141(68-74-170(299)300)194(321)261-148(94-122-98-232-126-50-24-23-49-124(122)126)199(326)258-143(89-111(2)3)196(323)247-134(58-32-40-83-223)189(316)262-149(96-160(226)285)180(307)235-100-161(286)233-104-165(290)274-85-42-60-156(274)207(334)267-154(108-280)206(333)265-151(105-277)181(308)237-101-162(287)239-117(12)213(340)276-87-44-62-158(276)214(341)275-86-43-61-157(275)208(335)268-153(107-279)204(331)249-132(56-30-38-81-221)187(314)246-131(55-29-37-80-220)186(313)245-130(54-28-36-79-219)185(312)244-129(53-27-35-78-218)184(311)243-128(52-26-34-77-217)183(310)242-127(176(227)303)51-25-33-76-216)272-201(328)146(92-120-45-19-17-20-46-120)260-197(324)144(90-112(4)5)257-190(317)135(59-41-84-231-215(228)229)255-209(336)172(114(8)9)271-177(304)116(11)240-182(309)138(65-71-167(293)294)251-192(319)139(66-72-168(295)296)252-193(320)140(67-73-169(297)298)253-195(322)142(75-88-342-15)254-191(318)137(63-69-159(225)284)250-188(315)133(57-31-39-82-222)248-203(330)152(106-278)266-198(325)145(91-113(6)7)259-200(327)150(97-171(301)302)263-205(332)155(109-281)269-212(339)175(119(14)283)273-202(329)147(93-121-47-21-18-22-48-121)264-211(338)174(118(13)282)270-164(289)103-236-179(306)136(64-70-166(291)292)241-163(288)102-234-178(305)125(224)95-123-99-230-110-238-123/h17-24,45-50,98-99,110-119,125,127-158,172-175,232,277-283H,16,25-44,51-97,100-109,216-224H2,1-15H3,(H2,225,284)(H2,226,285)(H2,227,303)(H,230,238)(H,233,286)(H,234,305)(H,235,307)(H,236,306)(H,237,308)(H,239,287)(H,240,309)(H,241,288)(H,242,310)(H,243,311)(H,244,312)(H,245,313)(H,246,314)(H,247,323)(H,248,330)(H,249,331)(H,250,315)(H,251,319)(H,252,320)(H,253,322)(H,254,318)(H,255,336)(H,256,337)(H,257,317)(H,258,326)(H,259,327)(H,260,324)(H,261,321)(H,262,316)(H,263,332)(H,264,338)(H,265,333)(H,266,325)(H,267,334)(H,268,335)(H,269,339)(H,270,289)(H,271,304)(H,272,328)(H,273,329)(H,291,292)(H,293,294)(H,295,296)(H,297,298)(H,299,300)(H,301,302)(H4,228,229,231)/t115-,116-,117-,118+,119+,125-,127-,128-,129-,130-,131-,132-,133-,134-,135-,136-,137-,138-,139-,140-,141-,142-,143-,144-,145-,146-,147-,148-,149-,150-,151-,152-,153-,154-,155-,156-,157-,158-,172-,173-,174-,175-/m0/s1

(4S)-5-[[2-[[(2S,3R)-1-[[(2S)-1-[[(2S,3R)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-5-amino-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S,3S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-4-amino-1-[[2-[[2-[(2S)-2-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[(2S)-2-[(2S)-2-[[(2S)-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[[(2S)-6-amino-1-[[(2S)-1,6-diamino-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidine-1-carbonyl]pyrrolidin-1-yl]-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]carbamoyl]pyrrolidin-1-yl]-2-oxoethyl]amino]-2-oxoethyl]amino]-1,4-dioxobutan-2-yl]amino]-1-oxohexan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-3-methyl-1-oxopentan-2-yl]amino]-1-oxo-3-phenylpropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-5-carbamimidamido-1-oxopentan-2-yl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-carboxy-1-oxobutan-2-yl]amino]-4-methylsulfanyl-1-oxobutan-2-yl]amino]-1,5-dioxopentan-2-yl]amino]-1-oxohexan-2-yl]amino]-3-hydroxy-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-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

AVE0010Adlyxin; Lyxumia; ZP10A peptide; Lixisenatide Acetate; 1997361-87-1; Lixisenatide acetate (320367-13-3 free base); ZP10 A peptide; ZP10-A peptide; AVE-0010; AVE 0010

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.

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

H2O: ~50 mg/mL (~9.6 mM)

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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Solubility in Formulation 1: 100 mg/mL (19.16 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.)