Feline immunodeficiency virus (FIV) is a member of the retroviridae family of viruses. It causes an acquired immunodeficiency syndrome (AIDS) in domestic and non-domestic cats worldwide, representing an important veterinary issue. Genome organization of FIV and clinical characteristics of the disease caused by the virus are similar to those of human immunodeficiency virus (HIV). Both viruses infect T lymphocytes, monocytes and macrophages, and their replication cycle in infected cells is analogous. Thus, infection of cats with FIV is also a useful tool to study and develop novel drugs and vaccines against HIV. Anti-retroviral drugs studied extensively in HIV infection have targeted different steps of the virus replication cycle: 1) intervention of host cell surface receptors and co-receptors; 2) inhibition of fusion of the virus membrane with the cell membrane; 3) blockade of reverse transcription of viral genomic RNA; 4) interruption of nuclear translocation and viral DNA integration into host genomes; 5) prevention of viral transcript processing and nuclear export; and 6) inhibition of virion assembly and maturation. Despite much success of anti-retroviral therapy in slowing HIV progression in humans, similar therapy has not been thoroughly investigated for FIV infection in cats. FIV capsid protein (CA) drives the assembly of the viral particle, which is a critical step in the viral replication cycle. During this step, the CA protein oligomerizes to form a protective coat that surrounds the viral genome. In this article we perform a large screening of four hundred molecules from our in-house library. We used an in vitro assembly assay of p24, combined with microscale thermophoresis to estimate binding affinity. This screening led to the discovery of around 5 novel hits to drug development and drug design for new antiviral drugs.