DPP4 (Dipeptidyl Peptidase 4)

DPP4 expression was assessed by qPCR in 22Rv1 and C4-2 cells treated with dasatinib or midostaurin at IC50 concentrations. On the contrary, DPP4 expression in both 22Rv1 and C4-2 was reduced after treatment with midostarin (p < 0.05). Our study establishes DPP4 as a multifaceted pan-cancer biomarker with prognostic significance and immunotherapeutic implications, particularly in prostate cancer.

P=N/A, N=84, Active, not recruiting, AdventHealth Translational Research Institute | Trial completion date: Jun 2025 --> Dec 2026

The DPP4 inhibitor linagliptin, which is used clinically, consistently suppressed EwS viability with elevated sensitivity under hypoxia, where there was increased cell death of SK-ES-1 cells...These findings suggest that NPY and DPP4 enhance EwS survival through autocrine/paracrine signalling while reducing monocyte viability. Thus, targeting the NPY/DPP4 signalling axis may provide therapeutic benefit by directly suppressing EwS growth and enhancing efficacy of immunotherapy.

To further elucidate its role in the development of MAFLD, we inhibited DPP4 activity with vildagliptin (VILDA) and analyzed the global transcriptomic changes and specific gene and protein gene expression of steatosis-associated genes with and without DPP4 inhibition...Our in vitro HLC-model reproduced the DPP4-dependent aspects of the disease and responded positively to VILDA treatment. Further elucidation of the role of DPP4 in the etiology of MAFLD and other diseases is warranted.

High frequencies of PD-L1+memory B cells, PD-1+DC and PD-1+naïve CD4+ T cells correlated with shorter progression-free survival, whereas normal levels of PD-1+transitional monocytes were associated with longer overall survival. Lesion-specific aberrant T cells and TME remodeling may drive MF severity and contribute to future immunotherapy.

In vitro, DPP4 overexpression in PDAC cell lines inhibited cell proliferation, induced G1-S cell cycle arrest, impaired mitochondrial respiration, and markedly sensitized cells to erastin-induced ferroptosis...ACSL4 knockdown rescued DPP4 overexpression-induced ferroptosis and lipid ROS accumulation. These results demonstrate that DPP4 acts as a positive regulator of ferroptosis in PDAC by stabilizing ACSL4, highlighting the DPP4-ACSL4 axis as a potential therapeutic target to enhance ferroptosis-based strategies against this aggressive cancer.

Moreover, DPP4 knockdown recapitulated the antiproliferative effects of quercetin. Collectively, these findings identify DPP4 as a functional therapeutic target for thyroid cancer and demonstrate that quercetin inhibits thyroid cancer cell proliferation through a DPP4-dependent mechanism.

This study presents an integrative pan-cancer framework linking CD26 expression to immune infiltration, together with in vitro observations in breast cancer cells, offering a comprehensive pan-cancer and experimental characterization of CD26. CD26 might be a novel prognostic biomarker candidate and therapeutic target to counteract tumor development in highly aggressive cancer.

Inhibiting the enzymatic activity of sCD26 with Sitagliptin significantly mitigated aGVHD and improved survival in late-infused female mice. Our study indicates that scheduling UCB transplantation in the early morning could be a simple and effective prophylactic strategy for aGVHD and that inhibiting sCD26 could be a promising therapeutic approach for late infusions.

CAR-intrinsic features, notably co-stimulatory domain choice, define the tonic NF-κB activation tone in resting CAR T cells. Metabolic refueling boosts these baseline states without overstimulation, suggesting it may be especially valuable for weaker CAR constructs. These findings provide a framework for tuning CAR T cell function through combinatorial design strategies targeting signaling and metabolism.

P1/2, N=118, Active, not recruiting, AstraZeneca | Recruiting --> Active, not recruiting | Trial completion date: Jul 2026 --> Mar 2027 | Trial primary completion date: Jul 2026 --> Mar 2027

In vitro, treatment with vildagliptin reduced the expression of Vimentin and the capacity for colony formation in H460 and LLC cell lines. The correlation of CD26 expression in lung adenocarcinomas and better patient survival, the antiproliferative effect on tumor cells by CD26 inhibition, and an altered EMT status give rise to the hypothesis that CD26 inhibitors impact the biology and clinical course of lung adenocarcinomas.