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Studies prodigiosin and pioglitazone effects on lung cancer immune signals

Observes how two small molecules may affect immune checkpoint proteins in lung cancer.

Plain-language title generated from the registry record
Registry title: Modulatory Effect of Prodigiosin or Pioglitazone on TIME and the Crosstalk to Immune-Checkpoint Protein(s)

Key facts

Where
Cairo, EgyptSee the site

Where in Egypt

  • Faculty of Pharmacy, Ain Shams University, Advanced Biochemistry Research LabCairo, EgyptNo longer taking part

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Trial details

Who runs it
Ain Shams University
Trial code
NCT06502249
Record updated
16 July 2024
Original description
Lung cancer is one of the most common and serious types of cancer. Lung tumor cells exploit immune checkpoint proteins (ICPs) to maintain immune tolerance and thus promote tumor progression and invasion. Inhibition of ICPs using antibody therapies is one of the most common approaches for the treatment of lung cancer. Unfortunately, these antibody-based therapies can lead to severe adverse events. Moreover, a significant number of patients do not respond to immune checkpoint inhibition due to tumor heterogeneity and the immunosuppressive tumor immune microenvironment (TIME). The use of small molecule targeted approach instead of antagonizing antibodies may have the potential advantage of being able to target multiple ICPs in TIME with a single agent as well as improved tumor distribution.Read full original descriptionShow less

Modulatory Effect of Prodigiosin or Pioglitazone on Tumor Immune Microenvironment and the Crosstalk to Immune-Checkpoint Protein(s)

Lung cancer is one of the most common and serious types of cancer. Lung tumor cells exploit immune checkpoint proteins (ICPs) to maintain immune tolerance and thus promote tumor progression and invasion. Inhibition of ICPs using antibody therapies is one of the most common approaches for the treatment of lung cancer. Unfortunately, these antibody-based therapies can lead to severe adverse events. Moreover, a significant number of patients do not respond to immune checkpoint inhibition due to tumor heterogeneity and the immunosuppressive tumor immune microenvironment (TIME). The use of small molecule targeted approach instead of antagonizing antibodies may have the potential advantage of being able to target multiple ICPs in TIME with a single agent as well as improved tumor distribution.

Inclusion: Adults over 50 years old with NSCLC.

Exclusion: Lung cancer patients with any cancer other than NSCLC; Lung cancer patients with incomplete data or incomplete histopathology diagnosis report.

ClinicalTrials.gov NCT06502249