The case shows the significance of following prolactin levels in children who are on risperidone therapy particularly those who are non-verbal or those who cannot communicate any discomfort. Clinicians are to remember that risperidone leads to hyperprolactinemia which can simulate pituitary malfunctions. Early identification, educating caregivers, and substitution of prolactin-stimulating drugs with prolactin-sparing ones like olanzapine will allow avoiding unnecessary investigations and enhancing the clinical and family outcomes.

P2, N=57, Not yet recruiting, Fiona Stanley Hospital

P2, N=216, Not yet recruiting, First Affiliated Hospital of Zhejiang University

P3, N=100, Recruiting, Blokhin's Russian Cancer Research Center

Palbociclib significantly enhanced this effect, while INK4C-IN-2 significantly reversed this blocking effect. In summary, we found a novel anti-tumor indication of antipsychotic drug perphenazine, which can inhibit the growth of tumor in vitro and in mouse-derived tumor model. These results suggested that perphenazine is also a promising anti-gastric cancer drug in clinical applications.

In AD-hBMI group, elevated thioridazine, 4-hydroxybenzaldehyde, and N-acetylleucine were positively correlated with ZO-1 level in CSF, reduced acesulfame and undecanoic acid were negatively correlated with OCLN level in CSF, and elevated (S)-S-methylcysteine sulfoxide was positiveiy correlated with both ZO-1 and OCLN levels in CSF. Elevated thioridazine and medroxyprogesterone were positively correlated with NO level in CSF, and decreased butyric acid was negatively correlated with ·OH level in CSF.ConclusionsHigh BMI may accelerate gut dysbiosis, leading to disrupted BBB, enhanced neuroinflammation, and ultimately accelerated cognitive impairment in AD patients.

Additionally, LUAD cell lines displayed consistent sensitivity signals for dropropizine (p = 8.47 × 10-3), terazosin (p = 1.11 × 10-3), morantel (p = 9.05 × 10-3), netilmicin (p = 8.37 × 10-3), altretamine (p = 9.82 × 10-3), and perphenazine (p = 9.58 × 10-3). Based on TP53-associated drug sensitivity profiles, this in silico analysis identifies atropine among the prioritized candidates, showing the strongest TP53-associated sensitivity signal in LUAD cell lines. Although experimental validation is required, the integration of independent computational datasets provides a robust framework for candidate prioritization and our findings provide a rationale for further preclinical investigation of atropine and related compounds in LUAD.

P2, N=288, Not yet recruiting, University Hospital, Strasbourg, France | Initiation date: Jan 2026 --> Oct 2026

P1, N=42, Recruiting, Intra-Cellular Therapies, Inc. | N=30 --> 42 | Trial completion date: Sep 2025 --> Jul 2026 | Trial primary completion date: Sep 2025 --> Jul 2026

Acute myeloid leukemia (AML) remains a therapeutic challenge due to high relapse rates and limited treatment options. Importantly, TFP synergized with venetoclax, a standard AML therapy, to enhance antileukemic efficacy both in vitro and in vivo. Collectively, our findings identify TFP as a potent ferroptosis inducer in AML and suggest its potential as a repurposed therapeutic agent, either as monotherapy or in combination with venetoclax.

P=N/A, N=2000, Completed, Shandong Cancer Hospital and Institute | Recruiting --> Completed

Compared with its precursor trifluoperazine, PTF exhibited markedly improved efficacy in inhibiting the proliferation of MCF-7 and MDA-MB-231 breast cancer cells, while sparing non-tumorigenic mammary epithelial cells (H184B5F/M10), which showed minimal sensitivity to the compound...Importantly, enforced expression of YAP attenuated PTF-induced cytotoxic effects, whereas blocking proteasomal function prevented PTF-driven degradation of YAP, implying that YAP destabilization contributes to the cytotoxic mechanism. Collectively, these results identify PTF as a potential therapeutic lead for breast cancer, acting through coordinated induction of apoptosis and autophagy, disruption of oncogenic signaling networks, and modulation of YAP protein stability.