Brd4884, MI192 and santacruzamate a

1. Brd4884, MI192 and santacruzamate a decreases senescence-associated beta-galactosidase in human cells.

   “They also improved nuclear architecture, reduced γH2AX signaling, preserved Ki67 positivity across serial passage, and limited senescence-associated β-galactosidase accumulation.”

   CellsHutchinson–Gilford progeria syndromevascular smooth muscle cell

   HDAC2 inhibition restores H4K16ac and delays senescence in HGPS VSMCs

   bioRxiv (Cold Spring Harbor Laboratory)·7 Nov 2025Preprint

More on Senescence-associated beta-galactosidase

1. Brd4884, MI192 and santacruzamate a decreases γH2AX signaling in human cells.

   “They also improved nuclear architecture, reduced γH2AX signaling”

   CellsHutchinson–Gilford progeria syndromevascular smooth muscle cell

   HDAC2 inhibition restores H4K16ac and delays senescence in HGPS VSMCs

   bioRxiv (Cold Spring Harbor Laboratory)·7 Nov 2025Preprint

More on γH2AX signaling

1. Brd4884, MI192 and santacruzamate a improves nuclear architecture in human cells.

   “They also improved nuclear architecture”

   CellsHutchinson–Gilford progeria syndromevascular smooth muscle cell

   HDAC2 inhibition restores H4K16ac and delays senescence in HGPS VSMCs

   bioRxiv (Cold Spring Harbor Laboratory)·7 Nov 2025Preprint

1. Brd4884, MI192 and santacruzamate a increases H4K16ac in human cells.

   “HDAC2-directed inhibitors (BRD4884, MI192, Santacruzamate A) restored H4K16ac in HGPS VSMCs, whereas the SIRT1 inhibitor EX527 did not.”

   CellsHutchinson–Gilford progeria syndromevascular smooth muscle cell

   HDAC2 inhibition restores H4K16ac and delays senescence in HGPS VSMCs

   bioRxiv (Cold Spring Harbor Laboratory)·7 Nov 2025Preprint

More on H4K16ac