Visterra has spent four years designing and fine-tuning an antibody that it thinks can combat all types of influenza. Now it’s pocketed some cash and filled out a revamped management team to take that drug into the clinic.
Cambridge, MA-based Visterra has added $8.1 million in venture dollars to its bank account, representing the third and final tranche from a $34.2 million Series A round that the company began raising last year. Existing investors Polaris Partners, Flagship Ventures, Lux Capital, the Bill & Melinda Gates Foundation, and Omega Funds provided the new cash, along with Visterra employees and executives. Visterra earned the latest tranche of cash by hitting certain “development and organizational” milestones, but CEO Brian Pereira wouldn’t disclose what those were.
Visterra has also added two new members to a rejiggered C-suite that amounts to a reunion of former Lexington, MA-based Amag Pharmaceuticals (NASDAQ: [[ticker:AMAG]]) executives: David Arkowitz, former Amag chief financial officer and chief business officer, is Visterra’s new chief financial officer and chief operating officer. Greg Miller, one-time Amag business development and corporate strategy head, is reprising a similar role as Visterra’s new vice president of business development and strategic planning. The two are rejoining Pereira, the former CEO of Amag, who took the head seat at Visterra in July.
The strategic shuffling comes at a critical time for Visterra, because it plans to put its first drug into clinical trials in the first quarter of 2014. The experimental drug, an antibody called VIS410, is the product of drug discovery engine developed by MIT bioengineering professor Ram Sasisekharan, whose lab work is also responsible for the creation of Momenta Pharmaceuticals (NASDAQ: [[ticker:MNTA]]) and Cerulean Pharma.
That technology essentially allows Visterra to get very detailed looks at what Pereira calls the “constrained” region of an epitope, a site on the surface of a virus that it uses to bind to, and infect cells. What makes the region of the epitope “constrained” is, it doesn’t mutate over time along with the rest of the virus. This means that if you could hit that specific area with an antibody, the virus shouldn’t be able to grapple on to a cell, regardless of which strain it is, or how it has mutated. By homing in on these areas, Visterra can gain access to “unique” drug target sites, study them, and design “broadly neutralizing” antibodies to hit them, according to Pereira.
VIS410 is the first product of that approach. It’s an engineered antibody that is supposed to hit
