clevudine moa the company also believes clevudine is unique in having better activity in reducing cccDNA, which could in theory contribute to better sustained response off therapy
fwiw if SVR does become a goal of future HBV therapy combinations with INF make sense (note inf is rarely used in HBV due to toxicity and modest efficacy, but it does have an sAg conversion rate and sustained response that is still better than nukes)
Clevudine does have a different MoA cause it primarily acts by blocking the HBV polymerase enzyme from incorporating nucleosides into a new viral DNA chain, whereas other antiviral agents compete with natural nucleosides for building HBV NDA chain and cause termination of the viral DNA.
Understood; what I’m alleging is that VRUS is exaggerating the practical consequence of Clevudine’s MoA. Rather than the handwaving that VRUS serves up to investors, I want to see hard data that Clevudine is different from other HBV nukes in a material way.
I’m skeptical that Clevudine monotherapy will generate the 40% SVR rate that VRUS claims to be seeking in the French study where Clevudine is going head-to-head vs Viread. If it can, I will of course be impressed.