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Tanshinone IIA absorption was poor, with an absolute bioavailability of 3. 5%. The poor absorption of Tanshinone IIA might have been brought on by its minimal aqueous solubility and restricted Aurora B inhibitor membrane permeability.

Most gene therapy trials for genetic diseases are aimed at sustained expression of therapeutic genes by introducing the vector into the target BI-1356 tissue with minimal or no tissue damage. Transduced cells and/or the expression of the therapeutic transgene following delivery of vectors are potentially able to trigger alloimmune responses involving both naive and memory lymphocytes, including lymphocytes specific for viral antigens. This scenario creates, to a certain extent, a clinical parallel to the immune responses following organ transplantation in which neoantigens in the graft are presented to the host immune system. To avoid allograft rejection, immunosuppression is required during the induction phase followed by a long term maintenance regimen.

Most of immune suppression strategies described in this review directed at avoiding adaptive immune response will also have an affect on the innate response to the gene delivery vector by BI-1356 decreasing inflammatory responses. The use of vector modified hematopoietic stem cell therapy in which myelocytotoxic and IS drugs are given to the host to create space in the bone marrow for the homing and expansion of gene corrected cells will not be reviewed. The immune systems reaction to antigen depends on the relative frequencies of responding T and B cells and on the thresholds of binding affinity that their receptors display, the levels of antigen present, and the period during which the antigen remains in secondary lymphoid tissue, where primary immune responses are initiated.

Deletion of T cells can occur when the cell is activated in the absence of co stimulation, or due to a lack of growth BI-1356 factors.