February 25, 2016 8:44am

Immunologic and reservoir analyses “suggest” mechanism for viral load control - BUY


 

SGMO presented immunological data from SB-728-T clinical trial, a ZFP Therapeutic® that provided functional control of HIV.

Analysis of data from Sangamo's most recent SB-728-1101 study suggests key, potentially interrelated mechanisms for viral load (VL) control in treated subjects during a treatment interruption (TI) from their antiretroviral therapy (ART).

The analysis was presented by SGMO's collaborator, Rafick-Pierre Sékaly, Ph.D., Richard Fasenmeyer Chair in Immunopathogenesis, Case Western Reserve University, at the 2016 Annual Conference on Retroviral and Opportunistic Infections (CROI 2016). The meeting is being held in Boston from February 22-26, 2016.

 

The Bottom Line: A significant number of subjects treated with SB-728-T have experienced a striking control of their viral load for a sustained period in the absence of ART. This is particularly notable in cohorts treated with optimal doses of Cytoxan® in the SB-728-1101 study. Immunological and HIV reservoir analyses suggest that the best predictors for post-treatment viral control are higher levels of SB-728-T engraftment, specifically long-lived memory T-cells, evidence of polyfunctional antiviral CD8 responses during TI and lower HIV reservoir levels prior to TI.

  • This may provide a model mechanism of action for SB-728-T and help identify HIV-infected individuals who will benefit most from this novel immune-based therapy;
  • The study was very encouraging.  In late 2015, Sangamo enrolled five additional subjects in Cohort 3* and expects to present that data at the end of 2016. Pending the data readout for SB-728-1101 Cohort 3*, the Company intends to partner the HIV program for pivotal studies and commercialization.

 

SGMO closed DOWN -$0.02 at $5.28. A positive indication however, strength seems to be sold into - BUY.

 

SB-728-T, is generated by zinc finger nuclease (ZFN)-mediated modification of the gene encoding the CCR5 receptor in a patient's own T-cells. ZFN modification disrupts the expression of this key co-receptor for HIV entry and renders cells resistant to HIV infection.