Altimmune Acquires NASH Drug Candidate via Spitfire Pharma Deal Worth Up To $93m

Jul 15, 2019 | Acquisition, ALT-801, GLP, NASH

NASH

Altimmune (ALT) acquired Spitfire Pharma in a deal that could ultimately be worth up to $93 million.

Some highlights of the deal include:

  • Company to receive rights to novel GLP-1/glucagon dual agonist that addresses obesity and metabolic dysfunction, primary causes of NASH
  • Greater impact on liver fat, inflammation and fibrosis compared to leading NASH candidates in established preclinical models
  • Altimmune plans to advance the drug candidate into the clinic during 2020
  • Company conducted conference call on Tuesday, July 9, 2019 at 8:30 a.m.

Altimmune, Inc. (Nasdaq: ALT), a clinical-stage biopharmaceutical company, today announced that it has entered into an agreement to acquire Spitfire Pharma, Inc. (Spitfire) including its product candidate SP-1373 (to be renamed ALT-801), a potent GLP-1/Glucagon receptor co-agonist for the treatment of non-alcoholic steatohepatitis (NASH). The transaction is expected to close during July 2019, subject to customary closing conditions.

Spitfire, a portfolio company of Presidio Partners, was founded by John J. Nestor, Jr., Ph.D. and Velocity Pharmaceutical Development, LLC, for the sole purpose of developing the NASH drug candidate, SP-1373. Spitfire shareholders will receive an upfront payment of $5 million in Altimmune common stock and will be eligible to receive an additional $8 million in future regulatory and clinical milestones payable in cash or common stock. Spitfire shareholders are also eligible to receive up to $80 million in sales-based milestones. The issuance of common stock to satisfy the milestone payments is subject to stockholder approval in accordance with Nasdaq rules.

“NASH is a significant unmet need. There are no approved treatments available, and prevalence is growing worldwide as a consequence of an expanding obesity epidemic. Compelling preclinical data generated by Spitfire suggests that ALT-801 could reverse obesity, a primary cause of NASH, thereby reducing excess liver fat, inflammation and fibrosis associated with the disease,” said Dr. Vipin K. Garg, Ph.D., President and Chief Executive Officer of Altimmune. “The addition of this exciting product candidate to our portfolio is a transformative transaction for Altimmune.”

ALT-801 builds on the Company’s liver disease expertise being developed in Altimmune’s HepTcellTM program for treating chronic hepatitis B and continues to build and leverage the Company’s deep knowledge of developing novel peptide-based therapeutics.

“We believe strongly in the potential of ALT-801 to become an important treatment for NASH and are excited to find a partner with the resources and experience to see this candidate through clinical development,” said David Collier, CEO of Velocity Pharmaceutical Development and Managing Director of Presidio Partners. “ALT-801 offers a compelling value proposition, and we look forward to participating in its advancement as shareholders of Altimmune.”

Conference Call and Webcast

Altimmune held a conference call and webcast to discuss this acquisition on Tuesday, July 9, 2019 at 8:30 a.m. Eastern Time. The conference call was accessible by dialing (877) 423-9813 (US/Canada) or (201) 689-8573 (International) and providing conference ID: 13692232. The call was webcast and is accessible from the company’s website at www.altimmune.com, under the “Investors” section.

A replay of the conference is accessible via the webcast link on the company’s website.

About ALT-801

ALT-801 is a potent, peptide-based therapeutic candidate with balanced agonist activity on the GLP-1 and glucagon (GCGR) receptors. ALT-801 is designed to treat the underlying metabolic dysfunction that leads to NASH, the most severe form of non-alcoholic fatty liver disease (NAFLD). NASH is considered by many to be the liver manifestation of metabolic syndrome and is characterized by abnormal accumulation of fat in the liver, toxic lipid metabolites, inflammation and liver cell damage leading to fibrosis/cirrhosis. ALT-801 acts upstream to block disease progression compared to most other NASH drug candidates in development, which instead focus on treating the liver damage that occurs as a result of NASH.

ALT-801 activates both the GLP-1 and the glucagon receptors, resulting in appetite suppression, decreased insulin insensitivity, increased energy expenditure, and substantial decreases in both liver and body fat in relevant animal models. ALT-801 has a similar mechanism of action to the body’s natural dual-acting hormone, oxyntomodulin, which lowers food intake, stimulates energy expenditure and reduces body weight. ALT-801 is designed to achieve glycemic control comparable to or better than the approved GLP-1 agonists but with more robust weight loss with once-weekly subcutaneous dosing.

ALT-801 demonstrated better outcome measures in comparison to semaglutide (an approved GLP-1 receptor agonist) or elafibranor (a PPAR alpha/delta agonist currently in development) in the Gubra/Amylin biopsy-proven, diet-induced mouse model of NASH. During this twelve-week study, treatment with ALT-801 rapidly returned body weight to the range of lean normal animals. Histology revealed a near complete absence of liver steatosis, lobular inflammation and ballooning as well as a significant reduction of fibrosis. Semaglutide showed a mild decrease in hepatosteatosis and modest body weight loss. Elafibranor also produced modest weight loss under these conditions, but historically this effect has not translated to weight decrease in clinical trials.

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