These results highlight tetrandrine's unique mechanism of action in enhancing MHC-I-mediated antigen presentation through dual inhibition of autophagic flux and proteasomal degradation. This study underscores tetrandrine's potential as a novel immunomodulatory agent to boost CD8+ T cell-mediated tumor cell eradication and enhance the efficacy of immune checkpoint therapies.

P4, N=32, Completed, Ain Shams University

The antitumor immunity mediated by tetrandrine and STING1 agonists is limited by neutralizing antibodies to the type I interferon receptor or CD8+ T cells. Thus, these findings establish a potential immunotherapeutic strategy against pancreatic cancer by preventing the autophagic degradation of STING1.

Ursodeoxycholic acid (UDCA) treatment is ineffective for certain cholestatic diseases like benign recurrent intrahepatic cholestasis (BRIC), despite increasing the hydrophilic bile acid pool. Additionally, Cil decreased the oxidative stress level compared with that in the ANIT-treated group. The results suggest that Cil effectively treats cholestasis by affecting the FXR signaling system and the NRF2 pathway.

Tetrandrine suppressed CM cell growth by triggering G0/G1 cell cycle arrest via IL-6/CDC42 inhibition. Tetrandrine should be a promising compound for CM treatment.

These differences resulted in differences in downstream actions, as KB-R7943 and nifedipine inhibited Rb1-mediated Ca2+ influx recovery only in MOVAS cells. In conclusion, Rb1 rescues the PA-induced Ca2+ influx by appropriately activating PLC in EA cells and PLD in MOVAS cells. This demonstrates that Ca2+ dynamics are elaborately regulated via intracellular Ca2+ signaling networks, suggesting a potential strategy for maintaining vascular Ca2+ homeostasis in hyperlipidemic environments.

P1, N=36, Not yet recruiting, City of Hope Medical Center

This study identified tetrandrine as a promising therapeutic candidate for attenuating macrophage activation associated with CAR-T cell therapy and LPS/Poly I:C-induced stimulation. These findings underscore the potential of tetrandrine to mitigate toxicities after CAR-T cell therapy while ensuring its therapeutic efficacy.

P1, N=30, Not yet recruiting, Merck Sharp & Dohme LLC

P1, N=24, Recruiting, Ohio State University Comprehensive Cancer Center | Suspended --> Recruiting | Trial completion date: Dec 2024 --> Dec 2027 | Trial primary completion date: Dec 2024 --> Dec 2025

P1, N=28, Recruiting, Ohio State University Comprehensive Cancer Center | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2024 --> Dec 2026

P2/3, N=126, Not yet recruiting, Deakin University

P2, N=183, Recruiting, American University of Beirut Medical Center | Trial completion date: Jan 2025 --> Jan 2026 | Trial primary completion date: Jan 2025 --> Jan 2026

P4, N=339, Completed, American Heart Association | Active, not recruiting --> Completed | N=3000 --> 339 | Trial completion date: Dec 2024 --> Jun 2024 | Trial primary completion date: Jun 2024 --> Jan 2024

This study highlights the potential of TET as an antimelanoma agent that targets SIRT5. These findings provide a promising avenue for the use of TET in melanoma treatment and underscore its potential as a therapeutic candidate.

P3, N=8518, Recruiting, Hospital Moinhos de Vento | N=12268 --> 8518 | Trial completion date: Dec 2026 --> Dec 2030 | Trial primary completion date: Dec 2025 --> Dec 2029

P3, N=180, Active, not recruiting, Rose Research Center, LLC | Recruiting --> Active, not recruiting | Trial primary completion date: Dec 2024 --> Mar 2025

This study also evaluates Tetrandrine (TET), a small molecule compound, as a potent CAMKIIδ inhibitor...Collectively, this study highlights how CAMKIIδ is critical in BCL progression. The results also pave the way for innovative therapeutic strategies for treating aggressive BCL.

P1/2, N=60, Recruiting, Global Neurosciences Institute | Phase classification: P1 --> P1/2 | N=20 --> 60 | Trial completion date: Apr 2023 --> Dec 2026 | Trial primary completion date: Apr 2023 --> Aug 2026

There was no significant difference between both groups in levels of other biomarkers. Three-months treatment with trimetazidine improved diastolic function parameters, LVGLS, dyspnea severity and LDL-C levels in diabetic patients with diastolic dysfunction.

The patient was initiated on nifedipine, which was gradually titrated. Subsequent ventilation-perfusion scan revealed chronic thromboembolic pulmonary hypertension (CTEPH), leading to anticoagulation therapy. We are reporting this case of PAH which presented with features of Group 4 PH and had a sarcoid-like reaction.

The antioxidant and anti-inflammatory effects of montelukast and trimetazidine were proved by the inhibition of malondialdehyde (MDA) and nitric oxide (NO) accumulation, with elevation of glutathione (GSH) and superoxide dismutase activity, decreased heat shock protein (HSP-70) expression, and a decline in interleukin-6 (IL-6) and tumor necrosis factor (TNF-α) levels in liver tissue. Also, the antifibrotic effects were explored by reducing levels of hydroxyproline and alpha-smooth muscle actin (α-SMA) expression in liver tissue and attenuating hepatic expression of hepatic expression of angiogenic mediator vascular endothelium growth factor (VEGF) and proliferative mediator Antigen Kiel 67 (Ki-67).

The reversal effect of the isoquinoline alkaloid coptisine (COP) was assessed on four breast cell lines; Two sensitive MCF-7 cell lines with positive estrogen, androgen, progesterone, and glucocorticoid receptors, as well as MDB-MB-231 cells with negative estrogen, progesterone, and HER2 receptors, and two doxorubicin-resistant cell lines, MCF-7/ADR and MDB-MB-231/ADR...The inhibitory effect of COP on ABCT efflux function in comparison to verapamil (VER) was evaluated by measuring the cellular accumulation of Rho123 using flow cytometry...The combination of COP and DOX had a strong inhibitory effect on ABCT function (3.1 and 3.9 times VER, P< 0.001) and downregulated the genes and protein expression of ABCT. COP reversed ABCT-mediated multidrug resistance in vitro, indicating its potential as a multidrug resistance-reversing agent in cancer chemotherapy.

P1/2, N=36, Completed, The University of Queensland | Not yet recruiting --> Completed

P2, N=27, Completed, Rennes University Hospital | Recruiting --> Completed

P3, N=750, Not yet recruiting, Milestone Pharmaceuticals Inc.

P4, N=92, Completed, Wake Forest University Health Sciences | Recruiting --> Completed | Trial completion date: Jun 2026 --> Nov 2024

P=N/A, N=12, Completed, Medical University of Vienna

The present research depicted that BIS and TMZ have the potential to protect the heart and provide therapeutic benefits by preventing acute heart injury induced by ATO. This is achieved by reversing the redox-sensitive pathway, reducing inflammation, and inhibiting apoptosis.

P1, N=55, Completed, University of Illinois at Chicago | Recruiting --> Completed | N=100 --> 55

P=N/A, N=618, Recruiting, Medical College of Wisconsin | Not yet recruiting --> Recruiting

P3, N=300, Recruiting, Medical College of Wisconsin | Trial completion date: Jun 2024 --> Jun 2025 | Trial primary completion date: Jun 2024 --> Jun 2025

Mechanistically, lacidipine targets calcium channels (CaV1.2/1.3) to inhibit Pyk2-JAK1-calmodulin complex-mediated IDO1 transcription suppression, which suppresses the kynurenine pathway and maintains the total nicotinamide adenine dinucleotide (NAD) pool by regulating NAD biosynthesis. These results reveal a new function of calcium channels in IDO1-mediated tryptophan metabolism in tumor immunity and warrant further development of lacidipine for the metabolic immunotherapy in breast cancer.

This study identified the role of key genes in thalamic hemorrhage-induced CPSP through snRNA-seq, providing a scientific basis for further exploration of the molecular mechanisms underlying CPSP.

P4, N=1, Completed, Vanderbilt University Medical Center | Enrolling by invitation --> Completed | Trial completion date: Jul 2025 --> Oct 2024 | Trial primary completion date: Jul 2025 --> Oct 2024

P=N/A, N=5047, Completed, Yuhan Corporation | Active, not recruiting --> Completed

P1/2, N=60, Recruiting, Minia University | Trial completion date: Nov 2024 --> Mar 2025 | Trial primary completion date: Nov 2024 --> Feb 2025

P=N/A, N=50, Not yet recruiting, Seoul National University Hospital

P2, N=2, Terminated, Marshall University | N=234 --> 2 | Trial completion date: Dec 2024 --> May 2024 | Recruiting --> Terminated; The study has closed due to difficulty in enrollment.

To lay the groundwork for the future rational optimization of this promising class of compounds, the molecular bases of DM1 and DM2 activity were investigated by modelling their interaction with hCav3.1 channels. The calculated binding modes of DM1 and DM2 to hCav3.1 channels partially mirrored that of the selective Cav3.1 blocker Z944, paving the way for future lead optimization.

P1, N=19, Completed, Merck Sharp & Dohme LLC

In conclusion, diltiazem shows promise as a protective agent for liver inflammatory diseases. Further research is warranted to translate these preclinical results into effective strategies for improving liver health.