A small-molecule class that binds to HIV particles to improve immune response and block viral entry into cells. Problem: 37 million people worldwide currently live with HIV and an estimated 2-3 million new infections occur annually. While antiretroviral therapies do exist for those with the disease, therapy interruption leads to the re-emergence of viral replication and disease progression. Hence, the inability to eradicate viral reservoirs presents a significant hurdle in finding a curative treatment for HIV. Furthermore, issues involving drug toxicity, and the potential for multidrug resistance limits effective therapies. Solution: The small molecule class works by binding to a specific component of HIV particles, preventing them from entering cells. It also sensitizes currently infected cells to our immune system, which is not normally possible during HIV infections. By preventing HIV from entering cells, the small molecules prevent the build-up of a viral reservoir. Furthermore, the involvement of the human immune system likely has fewer toxicity issues and less multidrug resistance than antiretroviral therapies. Technology: HIV uses envelope glycoprotein (Env) to bind to CD4 cell-surface receptors and enter cells. The structure of Env allows the virus to enter cells and avoid detection by antibodies. A high throughput screen revealed CD4-like small molecules that could interact with Env and change the structure such that the immune system could detect the virus. Assays that measure Env interaction and antibody-dependent cellular cytotoxicity (ADCC), helped identify a class of CD4 mimetic compounds (CD4mc). These compounds can change the structure of Env to improve the ADCC response from the human immune system. Advantages:
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Docket: 22-10087</rss.docket