Salicylate choline is a derivative of Aspirin (acetylsalicylic acid) and is orally active. It significantly reduces the levels of IL-1β, IL-6, TNF-α, and IL-10 in cells. By inducing S phase cell cycle arrest and impairing DNA damage repair, salicylate choline enhances the antitumor activity of the CRM1 inhibitor Selinexor (KPT-330). When combined with Selinexor, salicylate choline demonstrates excellent antitumor efficacy in mouse xenograft models with JeKo-1 cells. It is applicable in the research of rheumatism, inflammation, and cancer.

Salicylate choline significantly reduces levels of IL-1β, IL-6, TNF-α, and IL-10 in HGF-1 cells after 24 hours. In combination with Selinexor (KPT-330), Salicylate choline (2-3 mM, 48-72 hours) exhibits strong antiproliferative activity against hematologic malignancy cells, including MCL (JeKo-1, Mino), TCL (SR-786, Karpas-299), DLBCL (OCI-Ly1, OCI-Ly3, OCI-Ly19, SU-DHL-6, RPMI), MM (U266, OPM2, Xg1, KMS2), WM (BCWM, MWCL), ALL (RPCI, CRL-1783), and solid tumor cells such as pancreatic cancer (Panc-1, L3.6pl), non-small cell lung cancer (H460, A549, HCC827), small cell lung cancer (H1048), sarcoma (FuJi, SW872), and breast cancer (Hs 578T, BT-474, BT-20, MCF7). Moreover, Salicylate choline (3 mM, 24 hours) together with Selinexor significantly downregulates Rad51 and thymidylate synthase (TYMS) expression and increases γ-H2AX levels, a marker of DNA damage, in JeKo-1 cells. Additionally, Salicylate choline (3 mM, 24-48 hours) in conjunction with Selinexor after double thymidine block release significantly inhibits the expression of G2/M phase-related proteins (PLK1, Bub1b, Aurora A) in OCI-Ly1 cells (DLBCL).

In a xenograft model using male mice implanted with JeKo-1 cells, salicylate choline (500 mg/kg, oral administration, for 6 consecutive days each week over 26 days) in combination with Selinexor exhibited remarkable anti-tumor efficacy.