carbidopa

Mechanistically, high level of intracellular serotonin promotes histone serotonylation at H3K4me3Q5, reconfiguring the H3K4me3 chromatin landscape and downstream gene expression, which drives induced NE differentiation and is associated with suppressed androgen receptor signaling. Pharmacological inhibition of 5-HT synthesis using the FDA-approved DDC inhibitor carbidopa significantly impairs tumor growth and prolongs survival in both genetically engineered and patient-derived xenograft models, highlighting histone serotonylation as a druggable vulnerability in NEPC.

Peripheral blood mononuclear cells (PBMCs) from patients with PDAC and healthy donors were isolated and treated ex vivo with two AHR agonists (Carbidopa and Tapinarof) and one antagonist (BAY 2416964). Baseline AHR expression critically shapes the immune response to pharmacological modulation in PBMCs from PDAC patients. These findings suggest that AHR profiling may serve as a clinically relevant biomarker for stratifying patients and guiding personalized immunotherapy approaches for PDAC.

P2/3, N=30, Recruiting, University of Alberta | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Jun 2025 --> Jun 2026

P1/2, N=48, Not yet recruiting, Zhejiang Cancer Hospital; Zhejiang Cancer Hospital

Like carbidopa, taurine decreased alpha-synuclein, tumor-necrosis factor-α and interleukin-6 levels in the striatum and prefrontal-cortex. Additionally, taurine-reversed rotenone-induced neurodegeneration in the striatum and prefrontal cortex indicates neuroprotective function. Conclusively, taurine attenuates rotenone-induced PD-like behavior by enhancing the brain's antioxidant system, inhibiting pro-inflammatory cytokine release, reducing α-synuclein formation, and augmenting dopaminergic release in mice's brains.

Seizure frequency improved. This case highlights the utility of 18F-DOPA PET/MRI imaging in diagnosing focal hyperinsulinism beyond infancy.

P2/3, N=30, Recruiting, University of Alberta | Trial completion date: Dec 2024 --> Dec 2025 | Trial primary completion date: Jun 2024 --> Jun 2025

P1, N=35, Completed, Impax Laboratories, LLC | Recruiting --> Completed

P1, N=36, Recruiting, Impax Laboratories, LLC

The combination treatment significantly decreased the tumor size and volume compared to carbidopa and α-methyltryptophan alone. We do not know yet if the improved efficacy of the combination of the two drugs is due to a simple additive effect or due to a synergistic effect. Studies have shown that carbidopa promotes degradation of ER, indicating that carbidopa has its own independent anticancer effect that is relevant to ER-positive breast cancer.

In vivo, carbidopa suppressed the growth of ER-positive breast cancer cells in mouse xenografts; this was associated with increased apoptosis and decreased cell proliferation. Carbidopa has therapeutic potential for ER-positive breast cancer either as a single agent or in combination with other standard chemotherapies.

Mechanistically, we show that AhR is responsible for carbidopa-mediated suppression of IDO1, directly as a transcription factor and indirectly by interfering with the JAK/STAT pathway. Overall, targeting IDO1 not only in immune cells but also in cancer cells could be a beneficial therapeutic strategy for PDAC and potentially for other cancers as well and that carbidopa could be repurposed to treat cancers that overexpress IDO1.