
Heat shock protein 90 (Hsp90) accounts for 1-2% of the total proteins in normal cells and it functions as a dimer. Hsp90’s primary function is as a molecular chaperone that folds, assembles and stabilizes client proteins involved in cancer progression. Sansalvamide A, a novel hsp90 inhibitor, binds to the N-Middle domain of hsp90 and allosterically disrupts the binding of hsp90’s C-terminal domain proteins.1 Since hsp90 functions as a dimer, the dimerized sansalvamide A analog acts to inhibit the dimer of Hsp90. Utilizing our lead compound, Sansalvamide A 122 (San A 122)2, and a PEG linker, we developed several analogs of the dimerized sansalvamide A. Bioactivity study indicates that the PEG-9 dimer shows comparable ability to San A 122 in inhibiting hsp90’s chaperone function but enhanced effect on interfering the binding between hsp90 and its co-chaperones.