The Phase 1 study of BHV-1300 demonstrated up to an 84% reduction in total IgG, with a median reduction of 80%. How meaningful are these levels of IgG reduction in the treatment of autoimmune diseases, and how do they compare to existing FcRn inhibitors?

BHV-1300 showed rapid reductions in IgG levels within hours of administration, with sustained effects over four weeks. How does this profile influence its potential as a treatment option compared to other IgG-targeting therapies, and could this lead to less frequent dosing in future studies?

Unlike FcRn inhibitors, BHV-1300 selectively degrades IgG1, IgG2, and IgG4 while sparing IgG3, which plays a critical role in host defense. How important is this selectivity for maintaining immune protection, and could it offer an advantage in terms of infection risk compared to other IgG-lowering therapies?

The study reported that BHV-1300 was well tolerated at doses up to 2000 mg, with no severe adverse events or significant changes in liver enzymes, albumin, or cholesterol levels. What do these findings suggest about the drug’s safety profile, and what would you like to see in longer-term studies?

Biohaven plans to initiate a Phase 2 study of BHV-1300 in Graves’ disease, where IgG1 autoantibodies stimulate the thyroid. What makes Graves’ disease a promising target for this therapy, and what other autoimmune diseases might benefit from IgG degradation?

The study is continuing with dose escalation to explore deeper reductions and optimize the frequency of administration. What factors should be considered when fine-tuning the ideal balance between efficacy and safety for autoimmune disease patients?

Monoclonal antibody-based FcRn inhibitors have been a major focus in IgG-lowering therapies. How does BHV-1300’s small molecule degrader approach compare in terms of effectiveness, patient convenience, and potential long-term benefits?

With Biohaven planning to advance BHV-1300 into Phase 2 trials, what are the key regulatory considerations for bringing this therapy to market, and how could it reshape the treatment paradigm for patients with autoimmune diseases?