In today's Pharmaceutical Executive Daily, a pharma dealmaking roundup covers GSK's $750-million acquisition of a trispecific T cell-engager program from Chimagen Biosciences and Sanofi's expanded partnership with Cheplapharm, Stewart Gandolf discusses why pharma marketing now has to write for two audiences at once, and Dr. Elena Christofides explains why cortisol dysregulation may be the hidden reason some type 2 diabetes patients fail to respond to GLP-1 incretin therapies.
Two pharma dealmaking moves this week reflect continued consolidation in oncology and mature-medicine portfolios. GSK has agreed to acquire full global rights to a trispecific T cell-engager from Chimagen Biosciences for up to $750 million, adding a multiple myeloma candidate designed to bind T cells while targeting two tumor-associated antigens simultaneously, with Phase I trials expected to begin in 2027. Separately, Sanofi is expanding its partnership with Cheplapharm, transferring 20 mature medicines including Lovenox and three manufacturing sites in exchange for a 26.4% equity stake in the European specialty pharma company, with the transfer expected to complete by the third quarter of 2027.
Pharmaceutical Executive speaks with Stewart Gandolf, chief executive officer of Healthcare Success, on why pharma and biotech brands now have to write for two audiences at once: people and the AI systems increasingly mediating how patients search. Gandolf argues that heavy JavaScript, mandatory safety-information interstitials, and age-gates common on pharma sites can leave AI crawlers unable to "read" a drug's mechanism, eligibility, or efficacy data even when it's fully compliant, making a brand effectively invisible to the systems now doing the recommending. He contends that AI models tend to omit uncertain answers rather than risk an incorrect one, so silence is now the bigger risk for pharma brands navigating AI-driven search.
Finally, Pharmaceutical Executive speaks with Dr. Elena Christofides, scientific and medical advisor for Sparrow Pharmaceuticals, on why some type 2 diabetes patients fail to respond to GLP-1 incretin therapies despite favorable trial data. Christofides argues that undiagnosed cortisol dysregulation disrupts glucose signaling, insulin signaling, hormone integration, and fuel partitioning in a meaningful portion of patients, blunting or eliminating incretin drugs' effectiveness, and recommends the overnight dexamethasone suppression test as the only reliable way to screen for it. She contends that when a patient fails to respond, clinicians should first suspect a missed diagnosis rather than assume non-adherence.
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