This product is being developed as an entry inhibitor by the Japanese company Samjin. It inhibits HIV-1 entry once the virus is attached to the CD4 receptor at the cell surface. The exact mechanism is not known; it may be very similar to T-20's mechanism, acting by blockage of gp41 or another tertiary complex formed upon interaction of the virus and the cell.

Interestingly, once the virus is in the cell, SJ-3366 also acts as a non-nucleoside reverse transcriptase inhibitor (NNRTI). This was observed as a consequence of lack of SJ-3366 activity against HIV strains harbouring the Y181C, K103N or Y188C mutations on the reverse transcriptase gene, characteristic of the NNRTI class.

Mutants causing resistance to the penetration event are easily obtained, but those to the RT inhibition appear more difficult. SJ-3366 is synergistic with didanosine in cell culture protection studies. SJ-3366 has ~24% oral bioavailability in mice and a plasma half-life of 5 to 6 hr.

It belongs to the chemical class of pyrimidinedione.

Its IC₅₀ value is low (the IC₅₀ indicates the quantity of product necessary to inhibit 50% of the virus replication in vitro. The lower the IC₅₀ is, the more active the product, in vitro. Its selectivity index is >100,000 (you need more than 100,000 fold as much product to harm the cell than to inhibit the virus. SJ-3366 does not interact with any cellular protein, according to initial reports.

Its clinical development in humans has not started yet. Animal studies to evaluate its toxicity were due to start by February 2002.

Usually, Japanese biotech companies negotiate with larger pharmaceutical companies for the clinical development of their compounds. It is not known whether Samjin is already discussing development with any potential partner.