rosiglitazone

Cytotoxicity varied by compound, while the PPARγ agonist pioglitazone and the PPARα agonist fenofibrate were preferentially active in CTC lines, DG172 hydrochloride was selective for pleural effusion-derived lines, while rosiglitazone maleate, cloxiquine, and agrimol B showed no selectivity. These findings support PPARs as clinically relevant targets in SCLC, with PPAR-directed agents showing cytotoxic effects comparable to those reported in other malignancies. Such agents may aid SCLC treatment and help delineate biological differences between CTCs and resident tumor cells.

In addition, XFC partially reversed the effects of the PPARγ antagonist GW9662, activated the PPARγ signaling pathway, inhibited oxidative stress and inflammatory responses, and exerted anti-fibrotic effects similar to those of the PPARγ agonist rosiglitazone. XFC inhibits inflammation and oxidative stress by regulating the PPARγ/HMGCS2 pathway, thereby attenuating fibrosis and alleviating lung injury.

Our findings show that CEG therapy activates apoptotic PPARα and PPARγ genes and suppresses anti-apoptotic Bcl-2 and HIF-1Α genes, while reducing the oxidative stress and inflammation in EAC cells through a mechanism involving inhibition of NF-kβ. Finally, CEG creates a safe and synergistic environment that amplifies the therapeutic benefits of tamoxifen.

These findings contribute to the understanding of potential supportive strategies during doxorubicin-based chemotherapy. Further studies should be conducted to define appropriate dosing regimens, treatment durations, and to evaluate potential effects on cancer progression and patient outcomes.

With the approval of the antibody-drug conjugate enfortumab vedotin (EV), NECTIN4 has emerged as a bona fide therapeutic target in urothelial carcinoma (UC)...We demonstrate that the PPARγ pathway, critical for luminal differentiation, transcriptionally controls NECTIN4, and that the PPARγ agonist rosiglitazone primes and augments NECTIN4 expression, thereby increasing sensitivity to NECTIN4-CAR T cell-mediated killing. NECTIN4-CAR T cells have potent anti-tumor activity even against EV resistant cells, which largely retain NECTIN4 expression, including in a post-EV biopsy cohort. Our results elucidate a therapeutically actionable mechanism that UC cells use to control NECTIN4 expression and suggest therapeutic approaches that leverage PPARγ agonists for rational combinations with NECTIN4-targeting agents in UC, as well as future potential treatment options for EV-refractory patients.

A surgically induced KOA rabbit model evaluated the therapeutic effects of Sham US, US, Fenofibrate (PPAR-α agonist), and Rosiglitazone (PPAR-γ agonist) via MRI. By maintaining cartilage-chondrocyte equilibrium, US therapy prevented GW6471 or Mifobate's KOA-promoting impact. Our results show that US therapy could arrest the progression of KOA by reducing synovial inflammation, delaying cartilage degradation, and decreasing extracellular matrix degradation via PPARs-related signaling pathways.

Previously discovered bacterial depsipeptides (FR900359 and YM-254890) bind directly to Gαq and stabilize its inactive complex with GDP, but suffer from limitations of distribution and bioavailability...The thiazolidinedione analogs, rosiglitazone and pioglitazone, had no effect...SIGNIFICANCE STATEMENT: Troglitazone, unlike other thiazolidinediones, directly binds and inhibits activity of heterotrimeric G protein Gq, with a weaker effect on Gi. Troglitazone may find usage as a repurposed drug scaffold to build novel small-molecule Gαq inhibitors with better bioavailability than depsipeptide Gαq inhibitors.

The malignant progression of tumors could be inhibited using rosiglitazone and liraglutide combined with lipid-forming trans-differentiation therapy. In the field of bioinformatics, our study acquired genes characteristic of lipopolysaccharide-induced lung adenocarcinomas and elucidated for the first time that LPS-induced associated scoring patterns correlate with EMT progression. In addition, we propose the possibility of treatment with trans-differentiation therapies that utilize the high plasticity that EMT progressing cancer cells have.

Our results offer novel perspectives on the role of DNMBP-AS1/hsa-miR-30a-5p/PGC1α network in controlling CRC proliferation, metabolism and immune responses. Furthermore, our investigation reveals that using rosiglitazone combined with PGC1α agonist presents a promising therapeutic approach for managing CRC.

These findings advance our understanding of PPARG's regulatory network and underscore its potential as a therapeutic target, establishing a robust framework for future research in PPARG-related pathways.

Through Fe3+ -mediated one-step oxidative polymerization, PB and PPy were integrated into a hybrid nanozyme and further functionalized with rosiglitazone (PPAR-γ agonist) and rutin (tumor-targeting ligand)...In vivo, this platform completely inhibited 4T1 tumor growth, eradicated lung metastasis, and prevented recurrence (0% at 56 days) with an 80% long-term survival rate and no systemic toxicity. By unifying catalytic nanozyme design, PTEN-driven sensitization, and immune activation, this study establishes an interdisciplinary strategy to overcome resistance in PTT, offering a translatable approach for precision cancer therapy through tumor microenvironment modulation.

Overexpression of PCK1 inhibited cellular inflammation and fibrotic changes induced by pIgA1, demonstrating protective effects against cellular fibrosis similar to rosiglitazone. PCK1 exerted a pronounced inhibitory effect on mesangial cell inflammatory markers and fibrosis indicators in IgAN, potentially offering a novel therapeutic target for its treatment.