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Muthusamy, N.

Publications and source records attributed to Muthusamy, N..

2 recordsLinked to original sources

Design, Amino-Acid-Derived Analogues of FTY-720 and OSU-2S as PP2A Activators: Structure-Activity Relationships and Identification of Lead Compound XML-3D

Protein phosphatase 2A (PP2A) is a critical regulator of oncogenic signaling pathways, and pharmacological reactivation of PP2A through disruption of inhibitory protein interactions has emerged as a promising anticancer strategy. Although the sphingosine analogue FTY-720 and its derivative OSU-2S can restore PP2A activity, further structural diversification is needed to improve potency and expand structure-activity understanding. Here, we report the design, synthesis, and biological evaluation of three series of amino-acid-derived analogues incorporating tyrosine, homotyrosine, and tryptophan scaffolds. Docking models were used qualitatively to guide exploration of head-group functionality, hydrophobic tail variation, and stereochemical configuration; these models were hypothesis-generating and were not experimentally validated. Modular synthetic routes enabled efficient preparation of structurally diverse compounds from naturally occurring starting materials. Biological evaluation in leukemia and lymphoma cell lines revealed that hydrophobic tail length strongly influenced cytotoxic activity, while tryptophan-derived analogues were generally less potent than tyrosine-based scaffolds. Shortening the hydrophobic tail did not improve activity, contrary to the initial docking-based hypothesis. Stereochemical inversion at the amino alcohol head group yielded a lead compound, XML-3D, which demonstrated approximately two-fold enhanced cytotoxicity relative to FTY-720 and OSU-2S across leukemia cell lines (IC50 = 4.1, 1.8, and 1.5 uM in MV4-11, HL-60, and MEC-1 cells, respectively) and showed broader activity in mantle cell lymphoma lines (IC50 = 530 nM, 970 nM, and 110 nM in Jeko-1, Mino-1, and UPN1 cells). XML-3D induced increased PP2A phosphatase activity in cellular assays. Co-immunoprecipitation and pharmacological inhibition experiments were consistent with modulation of the PP2A/SET regulatory axis; however, direct binding measurements were not performed, and the mechanistic interpretation remains provisional. These findings suggest preliminary structure-activity relationships for amino-acid-derived PP2A modulators and identify stereochemical optimization as a productive direction for future development. Ongoing work aims to define molecular target engagement and refine mechanistic understanding to guide next-generation design.

molecular biology↗

Interleukin-10 suppression enhances T-cell antitumor immunity and responses to checkpoint blockade in chronic lymphocytic leukemia

T-cell dysfunction is a hallmark of B-cell Chronic Lymphocytic Leukemia (CLL), where CLL cells downregulate T-cell responses through regulatory molecules including programmed death ligand-1 (PD-L1) and Interleukin-10 (IL-10). Immune checkpoint blockade (ICB) aims to restore T-cell function by preventing the ligation of inhibitory receptors like PD-1. However, most CLL patients do not respond well to this therapy. Thus, we investigated whether IL-10 suppression could enhance antitumor T-cell activity and responses to ICB. Since CLL IL-10 expression depends on Sp1, we utilized a novel, better tolerated analogue of the Sp1 inhibitor mithramycin (MTMox32E) to suppress CLL IL-10. MTMox32E treatment inhibited mouse and human CLL IL-10 production and maintained T-cell effector function in vitro. In the E-Tcl1 mouse model, treatment reduced plasma IL-10 and CLL burden and increased CD8+ T-cell proliferation, effector and memory cell prevalence, and interferon-{gamma} production. When combined with ICB, suppression of IL-10 improved responses to anti-PD-L1 as shown by a 4.5-fold decrease in CLL cell burden compared to anti-PD-L1 alone. Combination therapy also produced more interferon-{gamma}+, cytotoxic effector KLRG1+, and memory CD8+ T-cells, and fewer exhausted T-cells. Since current therapies for CLL do not target IL-10, this provides a novel strategy to improve immunotherapies.

immunology↗