Lixisenatide
A short-acting GLP-1 receptor agonist originally approved for type 2 diabetes, now studied for slowing motor decline in early Parkinson's disease.
Lixisenatide is a short-acting, once-daily GLP-1 injection first approved for type 2 diabetes in 2016. Commercially it has essentially disappeared — Sanofi stopped selling it on its own in the US in 2023, and the EU authorisation was withdrawn in December 2025 — and the only product still on the market that contains it is a fixed combination with long-acting insulin. The reason people still talk about it is a 2024 trial suggesting it slowed motor decline in early Parkinson's disease. That result has not been confirmed, no follow-up trial has been registered, and the Phase 3 of its closest cousin failed.
What is Lixisenatide?
Lixisenatide (brand names Adlyxin in the US, Lyxumia in the EU) is a once-daily injectable GLP-1 receptor agonist originally FDA-approved in 2016 for type 2 diabetes. It is a 44-amino-acid peptide derived from exendin-4 (the same Gila monster venom peptide that exenatide is based on), with C-terminal modifications — removal of proline-38 and addition of six lysine residues — that improve receptor binding and half-life. Sanofi discontinued US marketing in 2023 for business reasons, but the peptide has since gained significant scientific attention for a very different reason: the 2024 NEJM-published LIXIPARK Phase 2 trial suggested it may slow motor decline in early Parkinson's disease, making it one of the most discussed GLP-1 repurposing candidates in neurology.
What Lixisenatide Is Investigated For
Lixisenatide is FDA-approved as a short-acting, once-daily GLP-1 receptor agonist for type 2 diabetes — notable for pronounced effects on gastric emptying that make it particularly effective for postprandial glucose control. The strongest evidence is the GetGoal Phase 3 program (~5,000 patients) showing HbA1c reductions of 0.5–0.9%, with the ELIXA trial (6,068 patients) establishing cardiovascular safety (neutral on MACE rather than protective). The most clinically interesting recent development is repurposing: the LIXIPARK Phase 2 trial (NEJM, 2024) showed the lixisenatide group had essentially no motor decline at 12 months while placebo declined 3.04 points on MDS-UPDRS Part III in early Parkinson's disease — a striking but small (n=156) signal, with Phase 3 still pending. Sanofi discontinued US marketing of Adlyxin in 2023 for commercial reasons (not safety), which makes the Parkinson's repurposing story the main reason lixisenatide remains in conversation. Weight loss effects are modest compared to newer weekly agents (semaglutide, tirzepatide), and the mean terminal half-life of approximately 3 hours means tolerability trade-offs differ from the long-acting GLP-1 class.
History & Discovery
Lixisenatide traces its lineage to exendin-4, the GLP-1-like peptide isolated from the saliva of the Gila monster (Heloderma suspectum) — the same starting point as exenatide. Originally developed by Zealand Pharma as AVE0010 and licensed to Sanofi, the molecule was engineered with two C-terminal modifications relative to exendin-4: removal of proline-38 and addition of six lysine residues, yielding a 44-amino-acid peptide with roughly 4-fold greater GLP-1 receptor binding affinity than native GLP-1. European approval as Lyxumia came in 2013; the FDA followed in 2016 with the Adlyxin brand. Sanofi voluntarily discontinued US marketing in 2023 for commercial reasons unrelated to safety — by that point the long-acting weekly agents (semaglutide, dulaglutide) had displaced short-acting once-daily GLP-1s in clinical practice. The molecule's second life began in April 2024 when the NEJM published the LIXIPARK Phase 2 trial showing slowed motor decline in early Parkinson's disease, making it one of the most-discussed neurology-repurposing candidates in the GLP-1 class.
How It Works
Lixisenatide mimics a natural gut hormone (GLP-1) that tells your pancreas to release insulin after meals, slows stomach emptying to reduce post-meal glucose spikes, and reduces appetite. For Parkinson's disease, the same receptors appear to exist in the brain, and activating them may protect dopamine neurons from ongoing damage — though exactly how this works is still being investigated.
Lixisenatide is a high-affinity GLP-1 receptor agonist with 4-fold greater receptor binding affinity than native GLP-1. Its short plasma half-life (mean terminal half-life approximately 3 hours after multiple dosing, per the FDA label and EMA SmPC) produces a pulsatile pharmacological profile quite different from long-acting GLP-1 agonists. Mechanistically, it augments glucose-dependent insulin secretion from pancreatic beta cells, suppresses glucagon release, delays gastric emptying (a pronounced effect with short-acting GLP-1s), and reduces appetite through central pathways. For Parkinson's disease, GLP-1 receptors are expressed on dopaminergic neurons in the substantia nigra, and preclinical models show GLP-1R activation reduces alpha-synuclein aggregation, neuroinflammation, and oxidative stress. The LIXIPARK trial hypothesis was that brain-penetrant GLP-1 stimulation could slow the neurodegeneration that drives Parkinson's motor decline. The exact mechanism — direct neuronal effects vs. microglial modulation vs. metabolic effects on neurons — remains an active research area. One caution about the foundation of this story: the 2012 BMC Neuroscience paper reporting that liraglutide and lixisenatide cross the blood-brain barrier and enhance neurogenesis, which is the most-cited source for lixisenatide's brain penetrance, received an Editorial Expression of Concern in October 2026 over image duplication, with readers advised to interpret its results with caution.
Evidence Snapshot
Human Clinical Evidence
Strong for T2D. The GetGoal program enrolled ~5,000 patients across multiple Phase 3 trials showing HbA1c reductions of 0.5-0.9%. ELIXA (6,068 patients) was the cardiovascular outcomes trial — neutral on MACE. For Parkinson's: LIXIPARK (2024, n=156, NEJM) is the key Phase 2 trial showing slowed motor progression; Phase 3 not yet initiated. A 2026 network meta-analysis (Neurol Sci, n=708 across 5 GLP-1 RA PD trials) places LIXIPARK in meta-analytic context with exenatide and liraglutide PD trials, and 2025/2026 preclinical work has extended the mechanistic case with lixisenatide-specific data on α-synuclein propagation. The class evidence has turned less favourable than the LIXIPARK headline implies. Exenatide-PD3, the Phase 3 trial of the closest sibling molecule, was null at 96 weeks (adjusted coefficient 0.92, 95% CI -1.56 to 3.39, p=0.47) and concluded there was no evidence to support exenatide as disease-modifying; note that the Lancet issued an Expression of Concern about that paper in June 2026. Two 2026 class meta-analyses were also null on the primary outcome: a four-trial analysis found no difference in MDS-UPDRS Part III off-medication (SMD -0.16, p=0.52) or on-medication (SMD -0.13, p=0.49), and the Neurol Sci network meta-analysis found no significant pairwise effect (MD -2.00, 95% CI -5.46 to 1.46) even though its dose-level network analysis did favour lixisenatide 20 mcg/day (MD -3.08, 95% CI -5.31 to -0.85). Separately, observational epidemiology consistently associates GLP-1 exposure with lower Parkinson's incidence — a Medicare cohort of 89,074 patients reported HR 0.77 in 2024, and a Scandinavian cohort reported HR 0.81 in 2026 — though lixisenatide accounted for a small fraction of exposure in those cohorts, so they are class evidence rather than lixisenatide evidence.
Animal / Preclinical
Strong. Extensive preclinical work on GLP-1 receptor agonism in Parkinson's models (MPTP, alpha-synuclein) consistently shows neuroprotection.
Mechanistic Rationale
Strong for diabetes (well-characterized GLP-1 biology). Moderate for Parkinson's — mechanism is plausible but exact pathway not fully established.
Research Gaps & Open Questions
What the current literature has not yet settled about Lixisenatide:
- 01Phase 3 confirmation of the LIXIPARK motor-progression signal. The 156-patient Phase 2 result is striking but small, and as of November 2026 no successor trial is registered: a ClinicalTrials.gov search returns exactly one lixisenatide Parkinson's study, LIXIPARK itself, completed. Two years on from a positive Phase 2 in a disease with no disease-modifying therapy, the absence of a registered Phase 3 is itself informative.
- 02Whether the observed motor benefit reflects true disease modification or a symptomatic effect is unresolved, and LIXIPARK's own design speaks to it more than the headline result suggests. The trial did include a 2-month washout after the 12-month treatment period. At 14 months, off medication, mean MDS-UPDRS motor scores were 17.7 (95% CI 15.7 to 19.7) with lixisenatide and 20.6 (95% CI 18.5 to 22.8) with placebo — confidence intervals that overlap. The washout therefore does not support a durable disease-modifying effect, and no biomarker endpoint was powered to settle the question.
- 03Effect on non-motor symptoms of Parkinson's disease (cognition, autonomic dysfunction, mood) — LIXIPARK did not demonstrate benefit on these domains.
- 04Optimal duration of therapy for neuroprotection — 12 months was studied; whether benefits accumulate, plateau, or require lifelong dosing is unknown.
- 05Mechanism of the Parkinson's effect — direct neuronal GLP-1R activation, microglial modulation, α-synuclein propagation effects, and peripheral metabolic effects on neurons are all candidates and not yet disentangled. A 2026 Trends Mol Med review (Santiago et al., PMID 41444101) proposed a multimodal biomarker-guided framework for GLP-1 agonists in neurodegeneration that would help address this gap, though it is written across Alzheimer's and Parkinson's rather than about LIXIPARK specifically.
- 06Whether the short-acting pulsatile pharmacokinetic profile is mechanistically preferable to long-acting weekly GLP-1 agonists for neuroprotection, as some commentators have hypothesized.
- 07Long-term immunogenicity — antibody formation has been observed and may reduce efficacy over time, but the long-term clinical consequence beyond the trial windows is unclear.
Forms & Administration
Subcutaneous injection once daily via pre-filled pen. Standard dosing for diabetes: 10mcg daily for 14 days, then increased to 20mcg daily. Administered within 1 hour before the first meal of the day. For Parkinson's research use (LIXIPARK trial): same dosing schedule (10mcg for 14 days, then 20mcg daily) for 12 months.
Dosing & Protocols
The ranges below reflect protocols commonly discussed in the literature and by clinicians — not a prescription. Actual dosing for any individual should be determined by a qualified healthcare provider who knows the patient.
Typical Range
For type 2 diabetes, the approved regimen is 10 mcg once daily for 14 days, then an increase to the 20 mcg once-daily maintenance dose. There is no higher approved dose; 20 mcg is the ceiling, which is one reason weight effects are modest relative to agents that titrate much further. In the fixed-ratio combination (Soliqua 100/33 in the US, Suliqua in the EU) lixisenatide is not dosed independently — the pen delivers 15 to 60 units, and the maximum daily dose of 60 units supplies 60 units of insulin glargine together with 20 mcg of lixisenatide. The LIXIPARK Parkinson's protocol used the diabetes schedule unchanged: 10 mcg daily for 14 days, then 20 mcg daily for 12 months.
Frequency
Once daily by subcutaneous injection, within the hour before the first meal of the day. This is not an arbitrary convention — the drug's main glycemic contribution is blunting the post-meal glucose rise through delayed gastric emptying, so timing it to a meal is how the effect is obtained.
Timing Considerations
Time of day
Once daily within the hour before the first meal of the day.
Relative to meals
Strictly pre-prandial. The postprandial glucose effect depends on the injection preceding food.
Relative to exercise
Not tied to exercise timing.
Cycle Length
Not a cycled drug. In type 2 diabetes it is intended for continuous use. In the Parkinson's setting the only human experience is 12 months of continuous dosing followed by a 2-month washout, and nothing is known about longer exposure.
Protocol Notes
Two practical points dominate. First, the gastrointestinal burden is front-loaded and substantial at this dose: nausea affected 46% and vomiting 13% of participants in the Parkinson's trial, which is high for a population taking the drug for a non-metabolic indication and with no glycemic benefit to offset it. Slower titration is the usual mitigation, but the approved schedule is already a two-step titration. Second, because the delay in gastric emptying is pronounced rather than incidental, it changes the absorption of anything swallowed near the injection — see drug interactions. Injection sites are the abdomen, thigh or upper arm, rotated. For the combination product, the pen's unit markings refer to insulin units, not micrograms of lixisenatide, which is a recurring source of confusion.
Lixisenatide is no longer marketed as a standalone product in the US or the EU, and it is not approved for Parkinson's disease anywhere. The schedules above describe approved diabetes labelling and the published trial protocol, not a recommendation.
Timeline of Effects
Onset
The gastric-emptying and postprandial glucose effects are present from the first doses — this is a short-acting agent with no accumulation phase, so there is no loading period. Nausea also appears early and is usually at its worst in the first days after each dose step.
Peak Effect
Fasting and postprandial glucose improve within the first weeks; the HbA1c effect, by the nature of the measure, takes roughly 12 weeks to express and reached 0.5 to 0.9 percentage points across the GetGoal trials. In the Parkinson's trial, the between-group motor difference was measured only at 12 months, and no earlier timepoint separated the groups in a way the trial was designed to detect.
After Discontinuation
With a terminal half-life of about 3 hours and once-daily dosing, glycemic effects are lost within about a day of stopping. The Parkinson's question is different and more interesting: after a 2-month washout at the end of LIXIPARK, off-medication motor scores were 17.7 with lixisenatide and 20.6 with placebo, with overlapping confidence intervals — consistent with the on-treatment difference having been at least partly symptomatic.
Monitoring & Measurement
Bloodwork & Labs
- •HbA1c — the registration endpoint in type 2 diabetes; expect 0.5 to 0.9 percentage points
- •Postprandial glucose, specifically after the meal following the injection — this is where a short-acting GLP-1 does its distinctive work and where a fasting-only check will miss the effect
- •eGFR and creatinine — lixisenatide is not recommended in severe renal impairment and has limited data there
- •Lipase or amylase only if pancreatitis is clinically suspected; routine screening is not recommended for the class
- •Anti-lixisenatide antibodies are measurable in research settings and have been associated with attenuated response, but there is no routine clinical assay or management pathway
Functional & Performance Tests
- •Body weight, as a secondary and modest effect rather than a treatment goal
- •For the investigational Parkinson's use, MDS-UPDRS Part III is the measure every trial has used; it is administered by a trained rater and is not a self-assessment
When to Test
In diabetes: baseline, then HbA1c at roughly 3-month intervals, with renal function at least annually and sooner in anyone with existing impairment.
Interpretation & Notes
There is no biomarker that tells you whether lixisenatide is doing anything neuroprotective. That is the central practical limitation of the Parkinson's story — LIXIPARK reported no disease-modification biomarker that separated the groups, and a 2026 review proposing a multimodal biomarker framework for GLP-1 agonists in neurodegeneration exists precisely because no validated marker does.
Common Questions
Is Lixisenatide still available?
Not on its own, anywhere. Sanofi discontinued US marketing of Adlyxin in 2023 and the FDA approval (BLA 208471, granted 27 July 2016) has not been withdrawn, but there is no current US prescribing information for it. In Europe the authorisation is gone outright: on 18 December 2025 the European Commission withdrew the marketing authorisation for Lyxumia at Sanofi Winthrop Industrie's request, after the company decided to permanently discontinue the product for commercial reasons. What does remain marketed is the fixed-ratio combination — Soliqua 100/33 in the US (insulin glargine plus lixisenatide, BLA 208673, approved 21 November 2016) and Suliqua in the EU — which is the only route by which a patient receives lixisenatide today. The renewed interest in the molecule stems from the 2024 LIXIPARK Parkinson's trial, not from commercial use in diabetes.
What did the LIXIPARK trial show?
Published in NEJM in April 2024, LIXIPARK was a 156-patient Phase 2 trial of once-daily lixisenatide versus placebo in early Parkinson's disease (<3 years from diagnosis). At 12 months, the lixisenatide group showed essentially no motor decline (−0.04 points on MDS-UPDRS Part III) while the placebo group declined by 3.04 points (p=0.007). Nausea (46%) and vomiting (13%) were common.
How does Lixisenatide compare to semaglutide or tirzepatide?
Lixisenatide is a short-acting, once-daily GLP-1 with a mean terminal half-life of about 3 hours — fundamentally different from the weekly long-acting agents like semaglutide (7-day half-life) and tirzepatide. It produces more modest weight loss but has pronounced effects on gastric emptying, making it particularly effective for postprandial glucose control. For Parkinson's, the short-acting pulsatile profile may actually be mechanistically preferred over continuous receptor stimulation.
Who Lixisenatide Is NOT For
- •Personal or family history of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2 (MEN 2) — a class-wide labeling caution for GLP-1 receptor agonists.
- •History of pancreatitis — pancreatitis is a recognized class effect and patients with prior episodes should generally avoid GLP-1 agonists.
- •Severe renal impairment — lixisenatide is not recommended in end-stage renal disease and has limited data in severe impairment.
- •Severe gastrointestinal disease such as gastroparesis — the pronounced gastric-emptying effect of short-acting GLP-1s can worsen symptoms.
- •Pregnancy and breastfeeding — safety has not been established and animal data signal potential fetal risk; the class is generally avoided.
- •Known hypersensitivity to lixisenatide or any exendin-based peptide.
Drug & Supplement Interactions
Because lixisenatide markedly delays gastric emptying, it can slow the absorption of co-administered oral medications — clinically meaningful for drugs with narrow therapeutic windows or where rapid onset matters (oral antibiotics, oral contraceptives, acetaminophen used acutely). Standard guidance is to take such oral drugs at least one hour before lixisenatide or to monitor response. Combining lixisenatide with sulfonylureas or insulin substantially raises hypoglycemia risk, and dose reductions of the sulfonylurea or basal insulin are commonly required when adding it. Beyond these, there are no well-characterized cytochrome-P450-based interactions, since lixisenatide is a peptide cleared by proteolysis rather than hepatic metabolism. For the investigational Parkinson's context, interaction data with dopaminergic therapies (levodopa, dopamine agonists) come only from the LIXIPARK trial population and no specific pharmacokinetic interaction has been described.
Safety Profile
Common Side Effects
Cautions
- • Not recommended in severe renal impairment
- • Risk of pancreatitis (class effect)
- • Antibody formation may reduce efficacy over time
- • Discontinued from US market by manufacturer (but not for safety reasons)
What We Don't Know
Long-term neuroprotective effects and optimal duration of therapy for Parkinson's disease remain unestablished. No Phase 3 trial of lixisenatide in Parkinson's disease has been registered — LIXIPARK (NCT03439943) is the only lixisenatide PD study on ClinicalTrials.gov, and it is complete — so 'Phase 3 pending' overstates what is actually underway. The 2024 trial did not demonstrate effects on non-motor symptoms or disease-modification biomarkers, and its post-washout motor scores did not separate from placebo.
Legal Status
United States
FDA-approved in 2016 as Adlyxin for type 2 diabetes; Sanofi voluntarily discontinued US marketing in 2023 for commercial reasons (the approval itself was not withdrawn for safety). Not approved for Parkinson's disease — that use remains investigational pending Phase 3 data after LIXIPARK.
International
Lyxumia was authorised in the EU on 1 February 2013, and the European Commission withdrew that marketing authorisation on 18 December 2025 at the marketing authorisation holder's request, for commercial reasons rather than safety. Standalone lixisenatide is therefore no longer available in the EU. The fixed-ratio combination with insulin glargine — Suliqua in the EU, Soliqua 100/33 in the US — remains authorised and is the only marketed product containing lixisenatide.
Sports & Competition
Lixisenatide is not named on the WADA Prohibited List (the 2026 list, or the 2027 list that takes effect January 1, 2027), and neither is any GLP-1 receptor agonist.
Regulatory status changes over time. Verify current local rules with a qualified professional.
Myths & Misconceptions
Myth
Lixisenatide was pulled from the US market because it was unsafe.
Reality
Sanofi voluntarily discontinued US marketing of Adlyxin in 2023 for commercial reasons — the long-acting weekly GLP-1s had taken over the diabetes market. The FDA approval was not withdrawn for safety concerns, and the ELIXA cardiovascular outcomes trial (6,068 patients) had previously established that lixisenatide did not increase cardiovascular event risk.
Myth
The LIXIPARK trial proved lixisenatide cures or reverses Parkinson's disease.
Reality
LIXIPARK was a 156-patient Phase 2 trial showing the lixisenatide group had essentially no motor decline at 12 months while placebo declined 3.04 points on MDS-UPDRS Part III. That is a slowed-progression signal, not reversal or cure, and Phase 3 confirmation is still pending. The trial also did not show benefit on non-motor symptoms or disease-modification biomarkers.
Myth
Lixisenatide is just a weaker version of semaglutide for weight loss.
Reality
It is a fundamentally different molecule in pharmacokinetics — a short-acting once-daily peptide with a mean terminal half-life of about 3 hours versus semaglutide's 7-day half-life. Weight loss is indeed more modest, but the pronounced gastric-emptying effect makes it particularly effective for postprandial glucose control, and the pulsatile profile may actually be the relevant feature for Parkinson's neuroprotection rather than a limitation.
Myth
All GLP-1 receptor agonists work the same way for Parkinson's disease.
Reality
They have produced genuinely different signals. Lixisenatide's Phase 2 was positive on its primary endpoint; exenatide's Phase 3 was null. The 2026 Neurol Sci network meta-analysis found no significant pairwise class effect yet did find dose-specific benefit for exenatide 20 mcg/day and lixisenatide 20 mcg/day, which is an argument that dose and molecule both matter. Two other 2026 meta-analyses pull in opposite directions — one found no motor benefit across four RCTs, another pooled eight trials and did find a small effect (SMD -0.21) plus mood and cognitive signals — so the class literature is not settled in either direction. Mechanism, brain penetration and pulsatile-versus-continuous receptor stimulation may all matter, and none has been isolated. Treating the class as interchangeable is unwarranted; so is assuming any one member works.
Published Research
16 studiesEditorial Expression of Concern: Drugs developed to treat diabetes, liraglutide and lixisenatide, cross the blood brain barrier and enhance neurogenesis
GLP-1 receptor agonists in Parkinson's disease: a meta-analysis revealing motor benefit and highlighting mood improvement.
Expression of Concern: Exenatide once a week versus placebo as a potential disease-modifying treatment for people with Parkinson's disease in the UK
Efficacy of GLP-1 receptor agonists in Parkinson's disease: a systematic review and exploratory network meta-analysis of randomized controlled trials
2026 Neurol Sci network meta-analysis of GLP-1 RAs in Parkinson's disease covering 5 RCTs (n=708) with MDS-UPDRS Part III as primary outcome. Provides the first meta-analytic context for the LIXIPARK lixisenatide signal alongside exenatide and liraglutide PD trials.
Use of Glucagon-Like Peptide-1 Receptor Agonists and Risk of Parkinson's Disease: Scandinavian Cohort Study.
Engström et al., Diabetes Obes Metab 2026. A Scandinavian cohort comparing GLP-1 receptor agonist users with sulfonylurea users: incidence rates of 5.2 versus 8.0 Parkinson's cases per 10,000 person-years, adjusted HR 0.81 (95% CI 0.68 to 0.96), consistent across lag-time and subgroup analyses. It is class-level epidemiology rather than lixisenatide evidence — liraglutide dominated the exposure time — but it is the methodologically strongest of the observational studies pointing the same way.
Efficacy and safety of glucagon-like peptide-1 receptor agonists in Parkinson's disease: a systematic review and meta-analysis of randomized placebo-controlled clinical trials
GLP-1 agonists in neurodegeneration: a multimodal biomarker-guided approach.
Neuroprotective effects of lixisenatide against propagation of α-synuclein pathology in Parkinson's disease
Exenatide once a week versus placebo as a potential disease-modifying treatment for people with Parkinson's disease in the UK: a phase 3, multicentre, double-blind, parallel-group, randomised, placebo-controlled trial
Exenatide-PD3 (Vijiaratnam et al., Lancet 2025) — the only Phase 3 test of a GLP-1 agonist in Parkinson's disease, and the essential context for reading LIXIPARK. 194 participants, 96 weeks, extended-release exenatide 2 mg weekly. MDS-UPDRS III off-medication scores worsened by 5.7 points on exenatide and 4.5 on placebo (adjusted coefficient 0.92, 95% CI -1.56 to 3.39; p=0.47), and the authors found no evidence to support exenatide as disease-modifying. The Lancet published an Expression of Concern about the paper in June 2026, so the result should be cited with that attached.
Are glucagon-like peptide-1 (GLP-1) receptor agonists useful in treating Parkinson's disease (PD)? Does the clinical trial with lixisenatide add anything?
Glucagon-Like Peptide-1 Receptor Agonists and Risk of Parkinson's Disease in Patients with Type 2 Diabetes: A Population-Based Cohort Study
Trial of Lixisenatide in Early Parkinson's Disease (LIXIPARK)
LIXIPARK — the 2024 NEJM RCT showing lixisenatide slowed motor-symptom progression in early Parkinson's disease over 12 months, the first positive disease-modification signal for a GLP-1 agonist in PD and the current most-cited reason for interest in the molecule.
Efficacy and safety of lixisenatide in a predominantly Asian population with type 2 diabetes insufficiently controlled with basal insulin: The GetGoal-L-C randomized trial (Yang et al., Diabetes Obes Metab 2018)
Lixisenatide: A New Daily GLP-1 Agonist for Type 2 Diabetes Management (McCarty et al., Ann Pharmacother 2017)
Lixisenatide in Patients with Type 2 Diabetes and Acute Coronary Syndrome (ELIXA)
ELIXA — the pivotal cardiovascular outcomes trial (NEJM 2015) establishing that lixisenatide did not increase cardiovascular event risk in post-ACS type 2 diabetes, the regulatory-defining CV safety study for the molecule.
Beneficial effects of once-daily lixisenatide on overall and postprandial glycemic levels without significant excess of hypoglycemia in type 2 diabetes inadequately controlled on a sulfonylurea with or without metformin (GetGoal-S) (Rosenstock et al., J Diabetes Complications 2014)
Quick Facts
- Class
- GLP-1 Receptor Agonist
- Tier
- C
- Evidence
- Strong
- Safety
- Well-Studied
- Updated
- Nov 2026
- Citations
- 16PubMed
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Clinical Trials
View Clinical TrialsLinks to ClinicalTrials.gov for reference. Listing does not imply endorsement.