metformin

P2, N=150, Not yet recruiting, Shandong Suncadia Medicine Co., Ltd.

In summary, our study elucidates that metformin inhibits sympathetic neuronal differentiation in PC12 cells by disrupting TrkA/ERK/EGR1 and p35/CDK5 signaling. This research contributes to uncovering a novel signaling mechanism in drug response during sympathetic neuronal differentiation, enhancing our understanding of the intricate molecular processes governing this critical aspect of neurodevelopment.

AM2 reduced lipogenesis and down-regulated the expressions of Clusterin, SREBP1 and FASN. These results suggest that AM2 inhibits the growth of bladder cancer cells T24 by inhibiting cellular lipogenesis associated with the Clusterin/SREBP1/FASN signaling pathway.

CMS and HFrEF seem to exacerbate Cfz-induced CAEs, by presenting metabolism-related hidden toxicity and PP2A-related cardiac inflammation, respectively. Metformin retains its prophylactic potential in the presence of CMS, while mitigating inflammation and Ca2+ signalling dysregulation in the HFrEF myocardium.

The results indicate that low-dose metformin can inhibit HCC metastasis by suppressing IL-8 expression. Targeting the AMPK/JNK/IL-8 axis may be a promising treatment strategy for patients with HCC metastasis.

Anti-cancer and cytotoxic effects of metformin can be effective in this strategy. In conclusion, the combination of conventional chemotherapeutic drugs, including SB203580, metformin, and takinib with X-ray exposure can be a new approach to diminish the drug resistance of breast cancer.

P3, N=1323, Completed, University of Minnesota | Active, not recruiting --> Completed

P2, N=388, Terminated, Semnan University of Medical Sciences | Unknown status --> Terminated; unfortunately due to COVID 19and social problems following it,we were unable to reach the estimated sample size.Evantually we could have only 151 patients .

P1/2, N=142, Completed, Gasherbrum Bio, Inc | Active, not recruiting --> Completed

In addition, they affected the expression of BCL2 and BAX genes and altered the cell cycle. Together, the combination of PCL-sorafenib/metformin and sorafenib/metformin increased sorafenib absorption at lower doses and also led to apoptosis and oxidative stress increases in MCF-7 cells.

P2, N=100, Not yet recruiting, Mayo Clinic

Moreover, paradoxical response of metformin may involve AMPK. Thus, metformin can mediate glioprotection due its effects on age-related disorders in non-diabetic and diabetic encephalopathy individuals.

In HR+/HER2-/PIK3CA-mutated ABC, prophylactic metformin before alpelisib plus endocrine treatment has low incidence and severity of alpelicib-induced hyperglycaemia. Novartis Pharmaceuticals.

P1, N=4, Terminated, Thomas Jefferson University | N=116 --> 4 | Trial completion date: Mar 2025 --> Mar 2024 | Active, not recruiting --> Terminated; Slow accrual

P=N/A, N=751, Completed, Singapore General Hospital | Active, not recruiting --> Completed

P2/3, N=60, Recruiting, Tanta University | Not yet recruiting --> Recruiting | Initiation date: Jan 2024 --> Apr 2024

Hyperglycemic male C57Bl/6 mice showed increased subcutaneous tumor development, partially inhibited by metformin...In summary, our findings show that a hyperglycemic environment stimulates murine melanoma B16F10-Nex2 primary tumor growth, and this effect is dependent on tumor cell stimulation, increased numbers of macrophages, and augmented IL-10 and NO concentrations. These findings show the involvement of tumor cells and other components of the tumor microenvironment in the development of subcutaneous melanoma under hyperglycemic conditions, defining novel targets for melanoma control in diabetic patients.

Furthermore, ZN8 produced a marked elevation in pAMPK and caspase-3 levels as well as a significant decrease in cyclin D1, COX-2, and PGE2 levels. The acquired findings verified the potency of MET-loaded ZNs as a treatment approach for BC.

The localization of the tumors in the area of the UV-exposed sites within the potential/actual contamination of the 4 preparations (simultaneously) in the described patient are indicative of a possible pathogenetic influence in the context of the already mentioned Nitroso-(Photo)carcinogenesis. Polycontamination of polymedication remains a so far unresolvable problem.

Drugs affecting cancer stem cells (CSCs) in OC, such as metformin and salinomycin, as well as inhibitors of CSCs markers aldehyde dehydrogenase 1 (with the drug ATRA) and the transcription factor Nanog homeobox (microRNA) are also discussed. A new approach to prevention and possible therapies under investigation such as development of vaccines containing a subpopulation of CD117(+) and CD44(+) stem cells with a promising option for use in women with OC was described.

P2, N=32, Completed, Singapore General Hospital | Recruiting --> Completed

Results indicated that metformin had a cytotoxic effect on ovary cancer cells and enhanced exosome biogenesis and secretion.

P2, N=60, Recruiting, Tanta University | Trial completion date: Mar 2025 --> Nov 2025 | Trial primary completion date: Mar 2024 --> Sep 2024

Our results establish PDECs as a feasible model to identify immunomodulatory functions of anticancer drugs in the context of patient-specific TIME.

P1, N=24, Completed, Jemincare | Active, not recruiting --> Completed

Metformin suppresses HIF-1α expression in CAFs to block tumor-stromal cross talk in breast cancer.

P4, N=4, Active, not recruiting, Christiana Care Health Services

P3, N=320, Recruiting, Eli Lilly and Company | Not yet recruiting --> Recruiting

P3, N=99, Active, not recruiting, Eli Lilly and Company | Trial primary completion date: Nov 2024 --> Aug 2024

P3, N=20, Active, not recruiting, Tufts Medical Center | Recruiting --> Active, not recruiting | N=36 --> 20

Participants with acromegaly or CD initiated long-acting pasireotide 40 mg/28 days intramuscularly (acromegaly) or pasireotide 600 μg subcutaneously twice daily during pre-randomization (≤16 weeks). Those who did not need antihyperglycemic medication, were managed with metformin, or received insulin from baseline entered an observational arm ending at 16 weeks...Increasing age, HbA1c, and FPG and pre-diabetes/diabetes were associated with increased likelihood of requiring antihyperglycemic medication during pasireotide treatment. These risk factors may be used to identify those who need more vigilant monitoring to optimize outcomes during pasireotide treatment.

Histopathological examination emphasizes the biochemical findings. The current investigation suggests that MTF-NPs might be considered as a potent novel treatment for the management of cardiac fibrosis and inflammation in patients who receive radiotherapy or workers who may be exposed to gamma radiation.

P3, N=555, Recruiting, HighTide Biopharma Pty Ltd

Metformin can reduce the level of INF-γ in tumor tissues, but JNK has no effect. Metformin can inhibit the expression of PD-L1 in triple-negative breast cancer mice and improve the tumor microenvironment, but does not reduce the size of the tumor.

P2, N=51, Not yet recruiting, Peking Union Medical College Hospital

This emphasizes the potential of targeting GJBs as a viable treatment approach for NSCLC patients receiving metformin.

P3, N=340, Active, not recruiting, Daewoong Pharmaceutical Co. LTD. | Not yet recruiting --> Active, not recruiting

To identify potential intestinal carcinogens, we developed a cell transformation assay (CTA) using mouse adult stem cell-derived intestinal organoids (mASC-IOs) and assessed the transformation potential on 14 representative chemicals, including Cd, iPb, Cr-VI, iAs-III, Zn, Cu, PFOS, BPA, MEHP, AOM, DMH, MNNG, aspirin, and metformin. Importantly, the activity of chemical-transformed mASC-IOs was associated with the degree of cellular differentiation of subcutaneous tumors, altered transcription of oncogenic genes, and activated pathways related to CRC development, including Apc, Trp53, Kras, Pik3ca, Smad4 genes, as well as WNT and BMP signaling pathways. Taken together, we successfully developed a mASC-IO-based CTA, which might serve as a potential alternative for intestinal carcinogenicity screening of chemicals.

P3, N=270, Recruiting, Novo Nordisk A/S | Not yet recruiting --> Recruiting

P4, N=1262, Recruiting, Novo Nordisk A/S | Trial primary completion date: Feb 2024 --> Jun 2025

P2/3, N=170, Active, not recruiting, Medical University of Vienna | Enrolling by invitation --> Active, not recruiting | Trial completion date: Nov 2022 --> May 2024 | Trial primary completion date: Oct 2022 --> May 2024

P1, N=256, Active, not recruiting, Genentech, Inc. | Recruiting --> Active, not recruiting