In this study the investigators will investigate the acute effects of increasing glucagon exposure on metabolic parameters in healthy participants.
Participants will participate in one study day. After initial baseline blood samples, a three-hour intravenous infusion with glucagon will be initiated. The infusion rate will be increased every 30 minutes.

Start Date01 Apr 2025

Sponsor / Collaborator

University of Copenhagen

NCT06424106

/ RecruitingNot ApplicableIIT

Effect of Glucagon on Fasting Insulin Secretion and Glucose Metabolism in Subjects Without Type 2 Diabetes

Fasting hyperglycemia contributes disproportionately to nonenzymatic glycosylation and the microvascular complications of type 2 diabetes. However, little is known about the regulation of glucose concentrations in the fasting state relative to what is known about the postprandial state. The proposed experiment is part of a series of experiments designed to establish how glucagon and insulin interact with their receptors to control fasting glucose in health and in prediabetes.

Start Date01 Apr 2025

Sponsor / Collaborator

Mayo Clinic

100 Clinical Results associated with Glucagon

100 Translational Medicine associated with Glucagon

100 Patents (Medical) associated with Glucagon

8,314

Literatures (Medical) associated with Glucagon

01 Dec 2025·PEPTIDES

Article

Author: Rasmussen, Christine ; Hansen, Caroline ; Ceutz, Frederik R ; Fisker-Andersen, Josephine ; Wewer Albrechtsen, Nicolai J ; Holst, Jens J ; Winther-Sørensen, Marie

Glucagon increases hepatic glucose production by activating both glycogenolysis and gluconeogenesis. Its effect on gluconeogenesis is traditionally attributed to increased expression of gluconeogenic enzyme genes. However, whether glucagon's transcription-independent actions are sufficient to acutely stimulate hepatic glucose output remains uncertain. To investigate this, we examined the acute effects of glucagon on hepatic gluconeogenesis using an in situ perfused mouse liver model. Livers from male, freely fed C57BL/6JRj mice (11-16 weeks) were perfused via the portal vein with oxygenated Krebs-Henseleit bicarbonate buffer. Hepatic glucose output was measured every three minutes. Glucagon (10 nM) added to the perfusate rapidly increased hepatic glucose production, with a 3.6-fold rise observed within minutes. This effect was absent in overnight-fasted mice. When gluconeogenic substrates (6 mM lactate, pyruvate, or both) were added to the perfusate, acute glucose production was stimulated. Co-administration of glucagon (10 nM) further enhanced glucose output by 36-43 % (p ≤ 0.044). Repeated stimulation experiments confirmed the reproducibility and reversibility of the response. These findings demonstrate that glucagon acutely and reversibly enhances hepatic gluconeogenesis, independent of transcriptional regulation and in the absence of hepatic glycogen. Our data redefine glucagon as a rapid metabolic modulator capable of minute-to-minute control of hepatic glucose output in the fasted state. This has important implications for our understanding of glucose homeostasis during fasting, stress, and disease, and challenges conventional textbook views of glucagon's role as solely a transcriptional regulator of gluconeogenic genes.

01 Dec 2025·Current gastroenterology reports

Review

Author: Arndt, Gretchen ; Jensen, Thomas ; Lindsay, Mark ; Wieland, Amanda

PURPOSE OF REVIEW:

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become the leading cause of chronic liver disease. This risk paralleled the rise in obesity rates, making MASLD a consequence of the Metabolic Syndrome (MetS). Until recently, clinicians have had limited pharmaceutical options in management this disorder. Glucagon-like Peptide 1 Receptor Agonist (GLP-1 RA) treatments have emerged as potential agents for noted benefits in many aspects related to the pathology and progression of MASLD.

RECENT FINDINGS:

Numerous trials including a recent Phase 3 trial utilizing GLP-1 RA based therapies have shown benefits for improvement in MASLD including MASH and fibrosis. Molecules that also act upon the glucose-dependent insulinotropic polypeptide (GIP) and/or glucagon have shown potential synergistic benefits in reversing inflammation and fibrosis. In summary, GLP-1 RA based therapies are being rigorously studied in management of MASLD in particular more advanced stages and likely will become foundational therapies in the future.

01 Dec 2025·MEDICINA CLINICA

Efectos de los fármacos con acción GLP-1 sobre las comorbilidades o enfermedades relacionadas con obesidad

Review

Author: Pellitero, Silvia ; Vilarrasa, Nuria

Agents targeting the glucagon-like peptide-1 receptor (GLP-1R) are effective in managing metabolic conditions associated with obesity, such as obstructive sleep apnea (OSA), metabolic dysfunction-associated steatotic liver disease (MASLD), and chronic kidney disease (CKD). In OSA, studies with first generation GLP-1R agonists (ArGLP-1) and co-agonists (GLP-1/GIP) have demonstrated significant improvements in the apnea-hypopnea index and weight reduction. In MASLD, GLP-1RAs and co-agonists (GLP-1/GIP or GLP-1/glucagon) have shown efficacy in reducing hepatic fat, improving fibrosis, and resolving steatohepatitis, with promising results from trials such as ESSENCE and SYNERGY-NASH. In CKD, semaglutide has been associated with a reduction in renal events and slower disease progression. Beyond their metabolic and cardiovascular benefits, these agents represent a comprehensive approach to treating obesity and its complications, with ongoing research exploring their potential indications in chronic inflammatory diseases such as psoriasis and hidradenitis suppurativa.

News (Medical) associated with Glucagon

11 Nov 2025

·ir.altimmune.com

Altimmune Announces Publication of IMPACT Phase 2b Trial Data in The Lancet and Concurrent Late-Breaking Oral Presentation at AASLD The Liver Meeting® 2025

24-week data demonstrated significant MASH resolution and weight loss, and strong evidence of anti-fibrotic activity with a favorable tolerability profile Significant improvements observed in secondary endpoints, including reductions in liver fat, inflammation and biomarkers of fibrosis GAITHERSBURG, Md., Nov. 11, 2025 (GLOBE NEWSWIRE) -- Altimmune, Inc. (Nasdaq: ALT), a late clinical-stage biopharmaceutical company developing novel peptide-based therapeutics for liver and cardiometabolic diseases, today announced publication in The Lancet of 24-week efficacy and safety data from the ongoing IMPACT Phase 2b trial of pemvidutide in patients with metabolic dysfunction-associated steatohepatitis (MASH) in a paper titled “Safety and efficacy of weekly pemvidutide versus placebo for metabolic dysfunction-associated steatohepatitis (IMPACT): 24-week results from a multicentre, randomised, double-blind, phase 2b study”. Dr. Mazen Noureddin, M.D., IMPACT trial principal investigator, Professor of Medicine at Houston Methodist Hospital and Co-Chairman of the Board for Summit and Pinnacle Clinical Research will present these data in a late-breaking oral presentation at The Liver Meeting® 2025, hosted by the American Association for the Study of Liver Diseases (AASLD) in Washington, D.C. Topline 24-week data from the IMPACT Phase 2b trial were previously announced in June 2025, demonstrating that pemvidutide, Altimmune’s 1:1 glucagon/GLP-1 agonist, achieved statistically significant MASH resolution without worsening of fibrosis, meaningful reductions in fibrosis, liver fat, and clinically relevant weight loss with favorable tolerability. The Lancet publication describes changes across key non-invasive tests (NITs) from blood-based biomarkers (ELF, PRO-C3, and AST), imaging modalities (MRI-PDFF, FibroScan®, and cT1), and combined measures such as FAST score – all markers that offer consistent evidence of fibrosis reduction and improvement in liver inflammation. “As the primary goal of treatment for patients with MASH is to reverse liver fibrosis to prevent progression to cirrhosis and other serious and life-threatening complications, the totality of the 24-week clinical data from the IMPACT trial is very encouraging,” said Dr. Mazen Noureddin. “Given the significant resolution of MASH that occurred after only 24 weeks of treatment, along with strong evidence of anti-fibrotic activity and weight loss, the profile of pemvidutide suggests it has the potential to meaningfully alter the course of this disease.” Highlights from the Published IMPACT 24-Week Results Endpoint Placebo (N=86) 1.2 mg (N=41) 1.8 mg (N=85) Primary Endpoint: Histology (ITT Analysis) MASH resolution without worsening of fibrosis, LSM % patients (SE) 20 (4.3) 58 (7.9) **** 52 (5.6) **** Fibrosis improvement without worsening of MASH, LSM % patients (SE) 28 (4.9) 33 (7.5) 36 (5.3) Secondary Endpoints Change in liver stiffness measurement, kPa (SE) -0.7 (0.5) -3.7 (0.7) *** -2.2 (0.5) * Change in Enhanced Liver Fibrosis score (SE) 0.03 (0.1) -0.6 (0.1) *** -0.5 (0.1) *** Change in corrected T1 relaxation time, ms (SE) -14.7 (11.9) -124.6 (16.1) *** -134.7 (11.9) *** Normalization of liver fat content (≤ 5%), n (%) patients 3/76 (4%) 12/39 (31%) **** 35/79 (44%) **** Body weight relative reduction, % (SE) −0.5 (0.3) −4.8 (0.5) *** −5.8 (0.3) *** Adverse Events (AEs) Adverse event leading to the discontinuation of treatment, n (%) 2 (2%) 0 (0%) 1 (1%) Any serious adverse event, n (%) 3 (3%) 1 (2%) 3 (4%) Serious adverse event considered by the investigator to be related to assigned treatment, n (%) 0 (0%) 0 (0%) 0 (0%) Data are presented as least squares mean (SE) unless indicated otherwise. A treatment policy estimand was applied with missing outcomes due either to missing biopsies or treatment discontinuations treated as non-responders (composite estimand). Comparisons versus placebo for the primary endpoints were made using the Chi-square test; **** p <0.0001 vs. placebo. The Cochran-Mantel-Haenszel test was applied to endpoints that were categorical in nature; **** p <0.0001 vs. placebo. Comparisons versus placebo were made using mixed models for repeated measures for endpoints measured at multiple time points and analysis of covariance for endpoints measured at baseline and week 24; * p <0.05, *** p <0.001 vs. placebo. “The dual glucagon and GLP-1 receptor agonism of pemvidutide, which has a unique, balanced 1:1 activity ratio, was intentionally designed to target both the hepatic and metabolic drivers of MASH. The strength of these IMPACT 24-week results, particularly the rapid resolution of MASH in 24 weeks, provides strong evidence for a reduction in fibrosis and significant reductions in other NITs, reinforcing our belief in the differentiated mechanism of pemvidutide and its potential to become an important treatment for patients with MASH,” said Christophe Arbet-Engels, M.D., Ph.D., Chief Medical Officer of Altimmune. “We also look forward to providing a final readout of longer-term NITs and weight loss from the IMPACT trial in the fourth quarter of 2025.” About the IMPACT Phase 2b Study The randomized, placebo-controlled, double-blind IMPACT Phase 2b trial (NCT05989711) enrolled 212 participants with biopsy-confirmed metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis stages F2 or F3, with and without diabetes. Study participants were randomized 1:2:2 to receive weekly subcutaneous pemvidutide doses at either 1.2 mg, 1.8 mg or placebo for 48 weeks. The primary efficacy endpoints, measured at 24 weeks, were MASH resolution without worsening of fibrosis, or fibrosis improvement without worsening of MASH. Secondary endpoints included non-invasive tests of fibrosis and weight loss. Participants will receive a total of 48 weeks of treatment, and a final readout of longer-term NITs and weight loss is anticipated in the fourth quarter of 2025. About Pemvidutide Pemvidutide is a novel, investigational peptide with balanced 1:1 glucagon/GLP-1 dual receptor agonist activity, in development for the treatment of metabolic dysfunction-associated steatohepatitis (MASH), alcohol use disorder (AUD) and alcohol-associated liver disease (ALD). The activation of glucagon results in direct effects on the liver, including reductions in liver fat, inflammation, and fibrosis, while GLP-1 receptors mediate metabolic effects such as appetite suppression and weight loss. The FDA granted Fast Track designations to pemvidutide for the treatment of MASH and AUD, both areas of significant unmet medical need. The 48-week readout from the ongoing IMPACT Phase 2b MASH trial is expected in the fourth quarter of 2025. Phase 2 trials in AUD (RECLAIM) and ALD (RESTORE) were initiated in May 2025 and July 2025, respectively, and are currently ongoing. About Altimmune Altimmune is a late clinical-stage biopharmaceutical company developing novel peptide-based therapeutics for liver and cardiometabolic diseases. The Company’s lead product candidate is pemvidutide, a glucagon/GLP-1 dual receptor agonist for the treatment of metabolic dysfunction-associated steatohepatitis (MASH), alcohol use disorder (AUD), and alcohol-associated liver disease (ALD). For more information, please visit www.altimmune.com. Forward-Looking Statements Any statements made in this press release related to the development or commercialization of pemvidutide, an investigational product candidate, and other business, regulatory and financial matters including without limitation, the timing of key milestones for the Company’s clinical assets, future plans or expectations for pemvidutide for the treatment of MASH, AUD, and ALD, and the prospects for receiving regulatory approval or commercializing or selling any product or drug candidates, are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. In addition, when or if used in this press release, the words "may," "could," "should," "anticipate," "believe," "estimate," "expect," "intend," "plan," "predict" and similar expressions and their variants, as they relate to Altimmune, Inc. may identify forward-looking statements. The Company cautions that these forward-looking statements are subject to numerous assumptions, risks, and uncertainties, which change over time. Important factors that may cause actual results to differ materially from the results discussed in the forward-looking statements, or historical experience include risks and uncertainties, including risks relating to: delays in regulatory review, manufacturing and supply chain interruptions, access to clinical sites, enrollment, adverse effects on healthcare systems and disruption of the global economy; the reliability of the results of studies relating to human safety and possible adverse effects resulting from the administration of the Company's product candidates; the Company's ability to manufacture clinical trial materials on the timelines anticipated; and the success of future product advancements, including the success of future clinical trials. Further information on the factors and risks that could affect the Company's business, financial conditions and results of operations are contained in the Company's filings with the U.S. Securities and Exchange Commission, including under the heading "Risk Factors" in the Company's most recent annual report on Form 10-K, quarterly report on Form 10-Q and the Company’s other filings with the SEC, which are available at www.sec.gov. Follow @Altimmune, Inc. on LinkedIn Follow @AltimmuneInc on X Investor Contact: Lee Roth Burns McClellan Phone: 646-382-3403 lroth@burnsmc.com Media Contact: Savannah Valade Real Chemistry altimmune@realchemistry.com This press release was published by a CLEAR® Verified individual. Source: Altimmune, Inc

Phase 2Clinical ResultFast Track

10 Nov 2025

·firstwordpharma.com

Camurus' monthly formulation of Wegovy leads to faster weight loss

As drugmakers push the weight-loss space beyond weekly incretin injections, investors seem to be intrigued by Camurus' FluidCrystal technology and its potential to create a version of Novo Nordisk's GLP-1 agonist Wegovy (semaglutide) that can be dosed monthly. Shares in the Swedish firm jumped close to 15% in Stockholm on Monday after it reported that CAM2056, its long-acting formulation of the obesity blockbuster, led to either comparable — or better — reductions in body weight, A1c and fasting glucose in an early-stage study. The Phase Ib trial enrolled 80 participants with overweight or obesity to receive either Wegovy, dosed according to prescribing information, or CAM2056 given every two weeks for two initiation doses, followed by two monthly doses. At day 85, patients taking 10 mg CAM2056 experienced mean weight loss of 9.3% from baseline, compared with 5.2% for weekly Wegovy. Essentially, the company explained, patients on weekly Wegovy took five months to achieve the same degree of weight loss as was reached by CAM2056 recipients in three months. In addition, the 10 mg CAM2056 cohort saw a mean A1c change from baseline of -0.44% at day 85, versus -0.12% for the Wegovy group.The safety profile of Camurus' formulation was consistent with weekly Wegovy, except for the cohort that received the highest, 5-mg initiation dose of the candidate, which saw more frequent and severe events. For all other cohorts, the company said, its tolerability profile was favourable, with mild-to-moderate and transient gastrointestinal symptoms being the most common adverse events. One to two patients per CAM2056 arm stopped treatment early, and two in the Wegovy group. "The study data suggest that CAM2056 allows rapid dose titration without compromising tolerability, whilst also allowing convenient monthly dosing," said Fredrik Tiberg, who serves as both chief executive and chief scientist of Camurus.The company plans to launch a Phase IIb trial next year that will test longer treatment durations and elevated doses.Monthly dosing goalAlthough Camurus is developing a monthly formulation of Wegovy, Novo Nordisk is working with a different firm to make its own once-a-month GLP-1 — and recently missed out on the opportunity to add one to its pipeline via M&A. Last year, Novo tapped Ascendis Pharma and its TransCon Carrier and Linker technologies to develop monthly weight-loss and diabetes drug candidates with sustained-release and prodrug properties. The Danish drugmaker had also made a surprise bid to buy Metsera and its ultra-long acting GLP-1 agonist MET-097i, but ultimately lost out to Pfizer (see – Vital Signs: Pfizer and Novo Nordisk battle for Metsera's pound of flesh).While Camurus doesn't have a deal with Novo, it's partnered with Eli Lilly to make long-acting versions of the US pharma's incretin portfolio, including dual GIP/GLP-1 receptor agonists and triple GIP/glucagon/GLP-1 receptor agonists.

Clinical ResultPhase 1Phase 2Acquisition

07 Nov 2025

·www.globenewswire.com

Altimmune Presents AI-Based Analysis of Liver Fibrosis Reduction from IMPACT Phase 2b Trial of Pemvidutide in MASH in Late-breaking Poster at AASLD The Liver Meeting® 2025

AI-based digital pathology analysis provides high-resolution quantification of hepatic fibrosis and objective measurement of fibrosis improvement Pemvidutide demonstrated significant reductions in liver fibrosis and improvements in non-invasive tests vs. placebo at 24 weeks GAITHERSBURG, Md., Nov. 07, 2025 (GLOBE NEWSWIRE) -- Altimmune, Inc. (Nasdaq: ALT), a late clinical-stage biopharmaceutical company developing novel peptide-based therapeutics for liver and cardiometabolic diseases, today announced results from an artificial intelligence (AI)-based analysis of biopsies from the IMPACT Phase 2b trial of pemvidutide in patients with metabolic dysfunction-associated steatohepatitis (MASH). The AI-based pathology tool Liver Explore™ showed that pemvidutide treatment resulted in significant reductions in the proportionate areas of early, advanced and total liver fibrosis compared to placebo at 24 weeks. These data are supported by significant improvements in non-invasive markers of fibrosis compared to placebo. The AI-based analysis will be presented on Saturday, November 8, in a late-breaking poster session at The Liver Meeting 2025, hosted by the American Association for the Study of Liver Diseases (AASLD) in Washington, D.C. “Changes in fibrosis can be difficult to quantify by traditional histological methods, which are semi-quantitative and prone to observer variability. AI-based methods can provide an automated, sensitive and truly quantitative analysis of changes in fibrosis in patients with MASH,” said Vlad Ratziu, MD, PhD, Professor of Hepatology at Sorbonne University and Pitié-Salpêtrière Hospital in Paris, France. “It is exciting to see this technology being used to accelerate the development of potential new therapies for MASH.” Highlights from the AI-based analysis of biopsies from patients in the IMPACT Phase 2b trial include: Data for total fibrosis showed 31% of patients in the pemvidutide 1.8 mg group (n = 85), and 12% of patients in the pemvidutide 1.2 mg group (n = 41) achieved a ≥ 60% reduction in the area of fibrosis compared to 8% of placebo-treated patients (n = 86, p = 0.0003 and p = 0.5, respectively). Data for early fibrosis showed 34% of patients in the pemvidutide 1.8 mg group (n = 85), and 24% of patients in the pemvidutide 1.2 mg group (n = 41) achieved ≥ 60% reduction in the area of fibrosis compared to 9% of placebo-treated patients (n = 86, p < 0.0001 and p = 0.017, respectively). Data for advanced fibrosis showed 27% of patients in the pemvidutide 1.8 mg group (n = 85), and 5% of patients in the pemvidutide 1.2 mg group (n = 41) achieved ≥ 60% reduction in the area of fibrosis compared to 11% of placebo-treated patients (n = 86, p = 0.0063 and p = 0.32, respectively). Additional analyses showed significant reductions in non-invasive tests (NITs) of liver fibrosis with pemvidutide compared to placebo, including in the PRO-C3:CTX-III ratio, consistent with fibrosis regression, and in PRO-C6, a fibrosis marker that may be linked to cardiovascular risk. “In our 24-week IMPACT MASH Trial, we achieved MASH resolution in up to 58% of patients, suggesting that the balanced 1:1 ratio of glucagon/GLP-1 in pemvidutide can lead to rapid MASH resolution,” said Christophe Arbet-Engels, M.D., Ph.D., Chief Medical Officer of Altimmune. “Using this powerful AI-based technology to examine liver biopsies, we found compelling reductions in total liver fibrosis as well, with statistically significant reductions in both early and advanced fibrosis (for 1.8 mg pemvidutide) at 24-weeks. We look forward to the upcoming 48-week IMPACT trial readout which will include longer-term NIT and weight loss data.” About the IMPACT Phase 2b StudyThe randomized, placebo-controlled, double-blind IMPACT Phase 2b trial (NCT05989711) enrolled 212 participants with biopsy-confirmed metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis stages F2 or F3, with and without diabetes. Study participants were randomized 1:2:2 to receive weekly subcutaneous pemvidutide doses at either 1.2 mg, 1.8 mg or placebo for 48 weeks. Key efficacy endpoints, measured at 24 weeks, were MASH resolution without worsening of fibrosis, or fibrosis improvement without worsening of MASH. Secondary endpoints included non-invasive tests of fibrosis and weight loss. Participants will receive a total of 48 weeks of treatment, and a final readout of longer-term NITs and weight loss is anticipated in the fourth quarter of 2025. About PemvidutidePemvidutide is a novel, investigational peptide with balanced 1:1 glucagon/GLP-1 dual receptor agonist activity, in development for the treatment of metabolic dysfunction-associated steatohepatitis (MASH), alcohol use disorder (AUD) and alcohol-associated liver disease (ALD). The activation of glucagon results in direct effects on the liver, including reductions in liver fat, inflammation, and fibrosis, while GLP-1 receptors mediate metabolic effects such as appetite suppression and weight loss. The FDA granted Fast Track designations to pemvidutide for the treatment of MASH and AUD, both areas of significant unmet medical need. The 48-week readout from the ongoing IMPACT Phase 2b MASH trial is expected in fourth quarter 2025. Phase 2 trials in AUD (RECLAIM) and ALD (RESTORE) were initiated in May 2025 and July 2025, respectively, and are currently ongoing. About AltimmuneAltimmune is a late clinical-stage biopharmaceutical company developing novel peptide-based therapeutics for liver and cardiometabolic diseases. The Company’s lead product candidate is pemvidutide, a glucagon/GLP-1 dual receptor agonist for the treatment of metabolic dysfunction-associated steatohepatitis (MASH), alcohol use disorder (AUD) and alcohol-associated liver disease (ALD). For more information, please visit www.altimmune.com. Forward Looking StatementsAny statements made in this press release related to the development or commercialization of pemvidutide, an investigational product candidate, and other business, regulatory and financial matters including without limitation, the timing of key milestones for the Company’s clinical assets, future plans or expectations for pemvidutide for the treatment of MASH, AUD and ALD, and the prospects for receiving regulatory approval or commercializing or selling any product or drug candidates, are forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. In addition, when or if used in this press release, the words "may," "could," "should," "anticipate," "believe," "estimate," "expect," "intend," "plan," "predict" and similar expressions and their variants, as they relate to Altimmune, Inc. may identify forward-looking statements. The Company cautions that these forward-looking statements are subject to numerous assumptions, risks, and uncertainties, which change over time. Important factors that may cause actual results to differ materially from the results discussed in the forward-looking statements, or historical experience include risks and uncertainties, including risks relating to: delays in regulatory review, manufacturing and supply chain interruptions, access to clinical sites, enrollment, adverse effects on healthcare systems and disruption of the global economy; the reliability of the results of studies relating to human safety and possible adverse effects resulting from the administration of the Company's product candidates; the Company's ability to manufacture clinical trial materials on the timelines anticipated; and the success of future product advancements, including the success of future clinical trials. Further information on the factors and risks that could affect the Company's business, financial conditions and results of operations are contained in the Company's filings with the U.S. Securities and Exchange Commission, including under the heading "Risk Factors" in the Company's most recent annual report on Form 10-K, quarterly report on Form 10-Q and the Company’s other filings with the SEC, which are available at www.sec.gov. Follow @Altimmune, Inc. on LinkedInFollow @AltimmuneInc on X Investor Contact:Lee RothBurns McClellanPhone: 646-382-3403lroth@burnsmc.com Media Contact:Savannah ValadeReal Chemistryaltimmune@realchemistry.com This press release was published by a CLEAR® Verified individual.

Phase 2Clinical ResultFast Track

100 Deals associated with Glucagon

External Link

KEGG	Wiki	ATC	Drug Bank
-	Glucagon	H04AA01	DB00040

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Diabetes Mellitus	Canada	Eli Lilly Canada, Inc.	25 Sep 2019
Hypoglycemia	United States	Eli Lilly & Co.	14 Nov 1960

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Diabetes Mellitus, Type 2	Phase 3	Japan	Eli Lilly & Co.	21 Feb 2018
Diabetes Mellitus, Type 1	Phase 3	Canada	Eli Lilly & Co.	01 Sep 2013
Common Cold	Phase 1	Canada	Eli Lilly & Co.	01 Mar 2013

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04992312 (RescuiNGkids, CTgov)	Phase 1	Diabetes Mellitus, Type 1	7	glucagon	tdglnplqyd = hqjsovvddv xltzpsmqil (ljdpohizln, htomydwhhf - hlwnwtiwew) View more	-	23 May 2024
Baqsimi (ESPE2022)	Not Applicable	HbA1c	68	Baqsimi® 3 mg	nqvvcesfoq(stgagqhoeg) = 21% bjopfftvxb (valkgurqpr ) View more	Positive	15 Sep 2022
NCT03970772 (Pubmed \| Diabetes Care)	Not Applicable	Diabetes Mellitus, Type 1	17	Mini-Dose Glucagon	tzfkfzvngf(wslospuzcv) = icfyyyxtrc khvyykotos (pjlkkopubp ) View more	Positive	17 Feb 2022
NCT02078726 (CTgov)	Phase 4	Colonic Cancer	100	Glucagon (Glucagon)	cllrivkcjm = xgeimycwpe ogoeslverw (oyegvjkolg, wofgdlepvn - fyhfjapmoz) View more	-	20 Apr 2021
				Glucagon (Placebo)	cllrivkcjm = pyoyepccgx ogoeslverw (oyegvjkolg, efoddgwgyd - pfbjxxwyzs) View more
NCT03533179 (Pubmed \| J Am Heart Assoc)	Phase 4	-	10	Esmolol+Saline	kpcpuxkkcq(jqyhsqdmwr) = ghpjcxddil xhwqmyycef (oibprbwpgj, 9.7 - 26.9) View more	-	03 Nov 2020
				Esmolol+Glucagon Bolus	kpcpuxkkcq(jqyhsqdmwr) = wyhosbpuhh xhwqmyycef (oibprbwpgj, 9.7 - 26.9) View more
NCT03421379 \| NCT03339453 (EASD2020)	Not Applicable	Hypoglycemia	-	Nasal glucagon	pmxswqqrey(utclcqpvyw) = urcafpqfxs drbhavmkha (cdyiqqtzel ) View more	Positive	24 Sep 2020
				Injectable glucagon	pmxswqqrey(utclcqpvyw) = kugbfzqfec drbhavmkha (cdyiqqtzel ) View more
NCT03421379 (Pubmed \| Diabetes Obes Metab) Manual	Phase 3	Diabetes Mellitus	75	Glucagon Nasal Powder	bsfrvvoyrt(pkoulvjeqk) = nypqtvjvui ocajzptvyr (qjmzmkcepy )	Non-inferior	01 Jul 2020
				Glucagon Hydrochloride Solution	bsfrvvoyrt(pkoulvjeqk) = drxtzmqsto ocajzptvyr (qjmzmkcepy )
NCT02806960 (CTgov)	Phase 1	Diabetes Mellitus, Type 2 \| Diabetes Mellitus, Type 1	12	Nasal Glucagon (Treatment 1)	xzpjxvuxaf(jhvxshlsnp) = grrypgldhr tanvhfejbx (xwfwkeriix, epnwzprgwn - xdnakmytwx) View more	-	13 Dec 2019
				Nasal Glucagon (Treatment 2)	xzpjxvuxaf(jhvxshlsnp) = qqbxhrlkxu tanvhfejbx (xwfwkeriix, hjaqjtmwyv - wrspmoaloy) View more
NCT02171130 (CTgov)	Phase 3	Hypoglycemia \| Diabetes Mellitus, Type 1	129	Nasal Glucagon	hmucgtgdyq = jncrxlkxnr doukbtqhml (iglcnsmmcd, nqpkyfqnmt - lihururutn) View more	-	15 Oct 2019
NCT02806973 (CTgov)	Phase 1	Diabetes Mellitus, Type 2 \| Diabetes Mellitus, Type 1	32	Glucagon (Nasal Glucagon Treatment 1)	ebvdqxsxys(bmgxhcxttq) = gfxnlmmkao wltbnaacji (xhzcyaokyd, 1850) View more	-	14 Oct 2019
				Glucagon (Nasal Glucagon - Treatment 2)	ebvdqxsxys(bmgxhcxttq) = inlspxvpqs wltbnaacji (xhzcyaokyd, 1760) View more

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