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Remember Carl June and his miracle blood cancer treatment?Remember Carl June announcing his miracle blood cancer treatment?
SGMO cured 3 of 8 heterzygotes. June will use cytoxan and messenger RNA and electroporation as a more efficient method offering higher rates of biallelic modifications of CCR5 than adenoviral delivery, which is what SGMO used. If, with cytoxan and mRNA, June gets up to 6 or 7 out of 8, I expect a miracle AIDs announcement. Note – his miracle cancer announcement came long before any IND.
SGMO on Heterozygotes In the SB-728-902 Cohort 5 study, bialleic modification of the infused CD4 cells could be approximately doubled by treating subjects heterozygous for the naturally occurring CCR5 delta-32 mutation. Three of eight evaluable CCR5 delta-32 heterozygous subjects with high levels of engraftment achieved a VL at or below the limit of quantification during a TI. This includes two of seven subjects that had initiated TI in the SB-728-902 Cohort 5 study and an additional CCR5 delta-32 heterozygote subject from an earlier Phase 1 clinical trial of SB-728-T. One SB-728-902 Cohort 5 subject, who had the highest levels of estimated biallelically modified cells and measurable immunological responses to the virus (polyfunctional anti-gag response), demonstrated sustained control of VL at or below the limits of detection, which is ongoing for more than 20 weeks into the TI.
Yesterday’s meeting:
In mid-September at ICAAC, we presented new data on demonstrating sustained control of viral load for well over a year without antiviral drug in a subject enrolled in our SB-728-902 cohort 5 Phase II trial. The subjects in this cohort already have one of that 2CCR5 gene disrupted and they represent approximately 5% to 10% of the U.S. HIV infected population.
While we had previously observed the decrease in viral load to undetectable levels in 2CCR5-delta32 heterozygous HVI infected subject. The data featured As Edward mentioned, we are and our collaborators are using the date that we’ve generated over these past trials to maximize the engraftment of cells that are being modified at CCR5 genes so called biallelic modification, which we have previously shown to be a significant driver in the treatment of control of viral load during the treatment interruption from antiretroviral therapy.
Cytoxan preconditioning prior to a single infusion of SB-738-T leads to a dose dependent increase in both engraftments CCR5 modified cells and notable increases in total CD4 cells above the baseline. In our dose ranging studies we determined of the optimal dose of Cytoxan was 1 gram per meter square. We also determined the delivery of the ZFNs used to knock out CCR5 gene by messenger RNA and electroporation is a more efficient method offering higher rates of biallelic modifications of CCR5 than adenoviral delivery, which is what we have used in our studies thus far
In contrast, Penn is proposing an open label Phase 1 study of single infusion of SB-728-T using electroporated messenger RNA with or without the prior administration of two different doses of Cytoxan. One cohort will not receive Cytoxan, two other cohorts will. In the Cytoxan treated group one cohort will comprise subject to CCR5 delta-32 heterozygote, the individuals who already have one CCR5 gene naturally mutated and the other Cytoxan pre-treated cohort will comprise a subject with both CCR5 genes intact or will undergo a 16-week treatment interruption. The purpose of both studies is to evaluate the |
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