Visterra Adds $8M, Ex-Amag Execs, To Begin Clinical Push for Flu Antibody

Xconomy Boston — 

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: 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: 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 a clustered group of amino acids on a protein called hemagglutinin, which researchers believe influenza viruses use to attach themselves to, and penetrate cells. Visterra believes that by blocking those amino acids, VIS410 has a chance to become a universal flu treatment—effective against seasonal and pandemic flu, as both a preventative and therapeutic treatment, and unaffected by the mutations that bedevil various vaccines and other methods.

“To me, this was the holy grail of influenza therapeutics,” Pereira says.

Still, this is early in the game. Though Visterra’s plan is to use a similar approach to amass a portfolio of treatments for other viruses and bacterial targets (such as Dengue Fever), it still hasn’t generated any evidence to date that its first drug works in humans—only preclinical signals in animals that have shown that VIS410 can effectively thwart a group of influenza A subtypes.

Further, it’s obviously not the only company trying to conquer the flu. Lots of big-name companies make flu vaccines, and are trying to find a universal one. And Crucell, the Dutch vaccine manufacturer acquired by Johnson & Johnson in 2011, is developing a flu antibody, as are a number of other smaller companies, according to Pereira. But Visterra thinks its technology has given it an edge.

“I think the scientific community would agree we are standing out because we have, in all of our preclinical experiments, shown that we cover both group 1 and group 2 [influenza strains] and that even some of the newer viruses that emerge, we are effective against those as well,” he says. With other technologies, Pereira says, “you cover some influenza viruses, not others, and even the existing influenza viruses have the opportunity to escape through mutation. That’s what differentiates us from the others in this field.”

Now it’s time to show it in the clinic, and that’s where the cash, and the new executive team, come in. Former CEO Steven Brugger led the company through its initial years of research and financing, and helped ink an antibody discovery deal with Pfizer in September 2012. But Pereira says that Visterra’s venture backers were looking for someone with experience with the type of tasks to come: taking VIS410 into clinical trials, prioritizing which antibodies to position behind it, and steering Visterra towards a return on the venture dollars poured into it.

“Right now we’ve got to get this train on its tracks and running,” he says.

So the VCs hired Pereira in July, and he’s now surrounded himself with some familiar faces. For Pereira, it’s a chance to bounce back from a rollercoaster five-year stint at Amag. On one hand, he helped Amag get its first drug, ferumoxytol (Feraheme)—an intravenous iron deficiency treatment for patients with chronic kidney disease—through clinical trials, approved by the FDA, and sold on the market. But on the other hand, the drug’s sales disappointed for various reasons, and Pereira responded with an ill-fated plan to merge the company with another struggling, single-product company, Allos Therapeutics. Shareholders vetoed the deal in late 2011, Amag restructured, and Pereira stepped down.

“When I look back, I think if the two companies had been merged with two products and a single cost base, it would’ve helped Amag do very well,” he says. “That also has taught me that sometimes, circumstances at a given time drive decisions that appear right at that point in time—but in retrospect, may not be the right course.”