A plausible MOA is always a plus when a medication is in early phase studies but our knowledge of the MOA, and more specifically the relative contribution of different mechanisms ascribed to the drug, almost always changes over time.
I ran across this interesting FDA publication with case studies of drugs reporting positive phase 2 studies (most better designed than the A273 2a) that went on to fail in phase 3. Besides a positive phase 2, practically every one had a reasonable MOA and positive preclinical data. For that reason, even with a medical and scientific background, I try not to get sidetracked on how great the MOA might be and put almost all of my effort dissecting available human clinical data. Interestingly, the text also offers good reason for the FDA's reluctance to rely on biomarkers in deference to well designed phase 3 studies with validated clinical endpoints.
Here's an excerpt from this FDA document: "Many medical conditions are complex; targeting a single component of a condition cannot be presumed to have a positive effect on the patient unless there is objective clinical evidence. This array of unexpected results from phase 3 studies demonstrates the complexity of the interaction between a medical product and the patient, and how logical presumptions without corroborating clinical evidence can be unreliable."
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