Based on the recent data from the ELVN-001 trials, how does the efficacy of ELVN-001 in achieving major molecular responses (MMRs) in CML patients compare to existing first-line therapies?

ELVN-001 has shown promise in patients previously treated with asciminib. Can you discuss the significance of this finding, particularly in the context of resistance management in CML therapy?

Considering ELVN-001's mechanism as a highly selective active site inhibitor, how does this contribute to its efficacy and safety profile, especially in comparison to other BCR-ABL tyrosine kinase inhibitors?

The treatment of CML patients with comorbidities can be challenging. How does ELVN-001's design cater to this patient population, and what impact might this have on their treatment outcomes and quality of life?

ELVN-001 has shown activity against the T315I mutation and resistance-conferring mutations to allosteric BCR-ABL inhibitors. How does this position ELVN-001 in the current landscape of CML treatment, particularly for patients with these challenging mutations?

In terms of patient convenience and adherence, how does ELVN-001 compare to existing treatments, given its design for potentially fewer stringent administration requirements?

With the ongoing Phase 1 clinical trial of ELVN-001, what are the key endpoints and study designs that clinicians and patients should be aware of?

Looking ahead, how do you envision the role of ELVN-001 in the future of CML treatment, and what are the potential implications for long-term disease management and patient prognosis?