Laid off from ImmunoGen, an ex-Genzyme and Shire exec heads to an ARCH upstart
ImmunoGen CBO Blaine McKee got laid off after the company had a big Phase III failure last March, but by the time his official exit came around in December, he already landed a plum new gig. ARCH Venture Partners had tapped the longtime executive to run a biotech willing to spend a lot of cash in an area that had gone under-invested: kidney disease.
Now that biotech is emerging from stealth mode with 12 employees, $51 million in Series A funding from ARCH and UCB Venture and two new methods of directly attacking a disease and an organ that drug developers have long only tried to mitigate from the side. They’ve also got a new name: Walden Biosciences.
“It’s horribly served, poorly served, there hasn’t been much innovation for years,” McKee told Endpoints News. “We’re not looking to slow the progression of renal diseases, we’re not looking to make a modest impact on renal disease, we want to full on stop or reverse the progression of renal disease.”
Although a couple recent upstarts have altered the picture, for years the majority of drugs in biotech pipelines have treated the chronic conditions that often trigger kidney diseases, CSO Alex Duncan noted. That’s been on particularly acute display over the past year, as AstraZeneca gradually rolled out what they’ve billed as “unprecedented” data on their SGLT2 diabetes drug Farxiga. Those data showed a 40% reduction in risk of kidney progression or cardiovascular death, but that was in patients regardless of diabetes status and in some ways an outlier.
“Pharma has tended to focus on, well, let’s treat the diabetes and we should be able to treat the kidney disease,” Duncan, a Medimmune and AstraZeneca vet who last worked at the cancer biotech Agenus, told Endpoints. “Well, that hasn’t happened.”
McKee, a longtime Genzyme executive who ran corporate development for Shire before the Takeda buyout, will direct a platform culled from the labs of Jochen Reiser and Sanja Sever at Massachusetts General Hospital and Harvard. Although they have yet to nominate lead candidates, their approach can be split into two different biological mechanisms.
In one path, they’ll look to target a protein known as soluble urokinase plasminogen activator receptor, or simply: suPAR. Researchers have known for years that the protein, when overproduced elsewhere in the body, can flow through the blood and cause harmful inflammation in the kidney. They’ve subsequently largely used it as a biomarker. But Walden says they can use antibodies to basically neutralize suPARs before they reach the kidney, returning it to normal levels — an approach akin to the antibodies now being developed to neutralize SARS-CoV-2 before it enters cells.
In the second path, they’ll look to activate a protein called dynamin. The protein helps support the physical structure of the kidney itself, and in a 2015 Nature Medicine paper, Sever and Reiser describe how a small molecule that continually activates the receptor can help maintain the kidney’s structure and ameliorate disease in animals. The approach, Duncan said, could allow patients to keep on meds they would have discontinued because of renal side effects.
“Even with the damage that might be being caused from conditions outside of the kidney, we can make the proper filtration apparatus inside,” Duncan said.
As they look to push the two programs, Walden will be boosted by a key regulatory change, McKee said. The FDA in 2018 changed their guidelines to allow companies to use the reduction of protein in the urine as an acceptable endpoint for accelerated approval. That, he said, could shave off years of development time.
They’ll be looking to put their first drug into the clinic in 2022.