One was PSMA-617 given at a standard dose every six weeks versus docetaxel also given at standard dose every three weeks for 12 cycles. Upon radiographic progression, patients were offered to be able to cross over and then they would receive the other arm of the treatment. And the patients were followed for RPFS-1, which was defined as from randomization to the time of first progression. And RPFS-2 was the second progression after crossover. The treatment arms were balanced in terms of clinical features, almost perfect symmetry between the groups. The dispositions of patients is outlined here. I won't have time to go into detail, but the key... It was fairly balanced in terms of patient's number, but the key finding though to remember when we look at overall survival is that there is significantly more patients who crossed over from the docetaxel arm to the PSMA-617 arm than the reverse. Many patients who underwent the PSMA-617 arm did not cross over to receive docetaxel, and we're going to publish even present hopefully at ASCO the reasons of why this happened and the implications of that on overall survival. Essentially, the primary endpoint of the study has been met. There's been a sufficient number of events, and the conclusion was that essentially the RPFS, the radiographic progression-free survival, between docetaxel and PSMA-617 in that patient group, the outcome was identical. Both curves are superimposed upon each other. And docetaxel, which is quite an effective treatment in the setting of metastatic prostate cancer, was very similar to PSMA-617. In terms of PSA response, PSMA-617 showed more prominent PSA response compared to docetaxel with a significant P-value.
And in terms of adverse events, apart from dry mouth, fatigue and surprisingly nausea, probably because antiemetics are not used in the PSMA-617 while they're routinely used for docetaxel, but the overall side-effect profile favored PSMA-617. The treatment was better tolerated than docetaxel, as you would expect from chemotherapy. Now, the RPFS-2, which integrates both the effects of the first-line treatment, as well as the crossover, showed no statistically significant difference between the two groups. So, the patients were doing well, whether you were doing similarly, not well, I have to correct. Similarly, whether you started with docetaxel or whether you started with PSMA-617. And the overall survival did show, however, a trend toward an advantage of patients who were first treated by the docetaxel. However, we do believe that this may not reflect the relative efficacy of the treatment, but more reflect the fact that more patients who were in the docetaxel group crossed over and received PSMA-617 and way fewer patients who received PSMA-617 crossed over into the docetaxel group. And it's well known that many patients, especially in Canada, they're not necessarily very keen to receive chemotherapy, and there's certainly some biases and so on. And we'll look into further details about why fewer patients crossed over. But I think the key thing to remember is there is that when patients follow all of the eligible treatments, they do tend to do a little bit better than when they stop short of some of the lines of treatments. And one of the obvious question as well is are patients who receive Pluvicto or PSMA-617 do better when they have high uptake of high SUVs on the baseline PET scans.
So, we looked into this and similarly to the VISION trial, we found that the SUV means, so this was made based on the same method that Hofman and colleagues did for the ENZA-p trial. We looked at the total tumor burden and the CSUV mean in those assessments. And it's not predictive for RPFS. It is a prognostic marker. So, patients who have higher SUVs tend to do better than patients who have lower SUVs, but it doesn't help predict whether they respond better to the docetaxel or PSMA-617. So just in conclusion, there was no difference in the primary endpoint. So, the RPFS was the same between whether you use docetaxel or PSMA-617 in patients who progress after ARPIs. Some of the endpoints favored PSMA-617, a higher proportion of patients with PSA decline in measurable disease response, fewer severe adverse events and treatment discontinuation in that group. The SUV mean was prognostic, but not predictive for PSMA-617 and docetaxel, and the overall survival was longer in patients initially randomized to the docetaxel. We do believe that this is possibly linked to the differences in crossover rates between the two arms. We are conducting additional analysis. We have an ongoing follow-up, longer follow-up, especially for patients who crossed over. Patient-reported outcomes are being monitored. We have further studies planned for PSMA PET parameters. Every patient got SPECT-based dosimetry in those cohorts, so we have quantitative dosimetry obtained for every patient in the trial at every cycle, and we collected ctDNA for all of these patient participants. And I think I gained us some time. Thank you.