Eh, so, guys, most group buy guys didn't PM me their email address, which makes me worried about whether they're still on board. I figure at least some of the absences are due to people not having realized yet the forum's back, so hopefully they'll trickle in, but if you are reading this, please do PM me just so I know you're still with us.
Did Cassiopea publish an actual paper on the dosing study, besides the results reported in the press release? I can't find one on Google Scholar.
By the way, this is not much, but a group of researchers including a guy who's worked on some Winlevi studies have published
a paper a few days ago about using CB-03-10 (note, not CB-03-01) as a potential treatment for tumors that have developed "GR-mediated resistance to AR blockade."
Overall, these preclinical findings support the selection of CB-03-10 for further development as an anticancer agent in cases where resistance to AR-targeted therapy or chemotherapy, via upregulation of GR activity, continues to limit the efficacy and duration of clinical benefit with these interventions.
This is of course wild speculation and BLATANT wishful thinking and grasping at straws on my part, but perhaps this is a bit of research that came out of AR blocking problems they came up against with Androgenetic Alopecia and that this is indication that they're working on the problem. Maybe this upregulation of GR activity is some indication as to why CB runs into problems?
Of course, I'm probably being silly here.
UPDATE: From the paper:
In addition to these mechanisms, a number of studies have shown that GR signaling can
potentially drive CPRC growth by activating a transcriptional program similar to the AR, thus
bypassing AR blockade (4-6). It has recently been documented that GR expression is
significantly increased following long-term ADT (androgen deprivation therapy) with abiraterone or enzalutamide (Enza) in a
number of preclinical models, indicating that GR upregulation is one possible mechanism of AR
resistance in CRPC (6). Therefore, despite the efficacy of anti-androgens in the short term, the
development of anti-androgen-resistant tumors in CRPC represents a significant challenge in the
treatment of advanced prostate cancer. GR can bind to and drive the expression of a subset of AR
target genes, thus allowing the cancer to progress despite ongoing AR blockade.
I don't know, I'm beginning to convince myself. We know that anti-androgen therapies that target hair loss also work on the prostate and the ARs there. This may be the same mechanism that's involved with CB.