Annexon Biosciences Closes $44 Million Series B Financing - Annexon Biosciences
	
	
	
	
	
	
	
	
	
	
	
	
	
















		
		

 



	
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Annexon Biosciences Closes $44 Million Series B Financing


June 23, 2016

Proceeds support advancement of clinical trials with lead candidates inhibiting the classical complement pathway in neurodegenerative disorders.

SOUTH SAN FRANCISCO, CA, June 23, 2016 – Annexon Biosciences, a biopharmaceutical company pioneering the development of classical complement pathway inhibitors to treat neurodegenerative disorders, today announced that it has closed a $44 million Series B financing. The Series B financing was led by new investor New Enterprise Associates (NEA), with participation by Correlation Ventures and existing Annexon investors, including Novartis Venture Fund, Clarus and Satter Investment Management, LLC. In conjunction with the financing, Frank Torti, M.D., a Partner at NEA, has joined the company’s Board of Directors.

“We welcome NEA to our world-class investor syndicate and Dr. Torti to our Board of Directors,” said Doug Love, Esq., Chief Executive Officer and President of Annexon. “This significant investment in our robust and risk-balanced pipeline further validates Annexon’s novel and elegant scientific approach. Moreover, the funding enables us to enhance and accelerate our biomarker-rich clinical development program in support of new and much-needed therapies for patients with serious neurodegenerative disorders.”

Annexon’s first-in-class pipeline of classical complement pathway inhibitors is focused on therapies for complement-mediated loss of nerve connections in the brain, as occurs in Alzheimer’s disease and Huntington’s disease, as well as in retinal cells, as seen in glaucoma. The Series B funding will be used to advance Annexon’s lead drug programs, including monoclonal antibodies ANX005 for serious central nervous system (CNS) and autoimmune disorders, and ANX007 for ophthalmic disorders. These lead therapeutic candidates inhibit a protein called C1q, the initiating molecule of the classical pathway, and block complement activation involved in neurodegeneration.

“In a short period of time, Annexon has effectively leveraged its novel anti-complement platform with therapeutic applications across a range of serious diseases supported by robust preclinical validation to date,” said Dr. Torti. “I am excited to be working closely with the leadership team and Board to advance the program through development in significant diseases of unmet need.”

Annexon was co-founded by Ben Barres, M.D., Ph.D., Professor and Chair of Neurobiology at Stanford University School of Medicine, and Arnon Rosenthal, Ph.D., Co-founder and Chief Executive Officer of Alector, and Co-founder, former President and Chief Scientific Officer of Rinat Neurosciences. Dr. Barres’ lab discovered the role of C1q in mediating synaptic removal in early development, as well as C1q’s role in the aberrant removal of functioning and otherwise healthy synapses as one of the first events in neurodegenerative disease. Working closely with expert research collaborators, Annexon has rapidly advanced first-in-class antibodies that inhibit C1q in the central and peripheral nervous systems in multiple neurodegenerative, autoimmune and ophthalmic disorders as shown in several recent scientific publications.

About Annexon

Annexon Biosciences is pioneering the development of first-in-class therapeutic products that halt the progression of complement-mediated neurodegeneration (CMND). Backed by a team of experts in CMND, Annexon’s mission is to rapidly advance disease-modifying therapies for patients with acute and chronic neurodegenerative disorders. Annexon’s antibody pipeline is based on breakthrough research involving the classical complement pathway and the unique role of its initiating molecule, C1q, in the loss of nerve connections, inflammation, and neuronal death. For more information, visit www.annexonbio.com.

Contact

MacDougall Biomedical Communications
Heather Savelle, 781-235-3060
hsavelle@macbiocom.com



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