metformin

Our results advocate for the potential of metformin as a viable therapeutic option for preserving ovarian function in cyclophosphamide-treated adolescent girls, given its favorable side effect profile and ability to improve cyclophosphamide-induced ovarian damage.

P=N/A, N=30, Not yet recruiting, University College Dublin

P1, N=200, Active, not recruiting, Genentech, Inc. | Trial completion date: Nov 2024 --> Dec 2026 | Trial primary completion date: Nov 2024 --> Dec 2026

P1, N=32, Completed, Boehringer Ingelheim | Active, not recruiting --> Completed

P2, N=30, Not yet recruiting, Boston Children's Hospital | Trial completion date: Oct 2027 --> Mar 2028 | Initiation date: Oct 2024 --> Mar 2025 | Trial primary completion date: Oct 2026 --> Mar 2027

P1, N=22, Completed, Washington State University | Active, not recruiting --> Completed

P4, N=890, Not yet recruiting, Peking University Third Hospital

Treatment with the AMPK agonist metformin significantly reversed the inhibitory effects of ImP on osteoblast differentiation and the promotion of adipocyte differentiation, along with enhanced AMPK (T172) phosphorylation. These findings suggest that the microbial metabolite ImP may disrupt bone homeostasis by stimulating p38γ phosphorylation and inhibiting the AMPK pathway, presenting a potential therapeutic target for managing metabolic bone diseases.

Drug sensitivity analysis suggested that Metformin, Gefitinib, and Lapatinib may be more effective in the low-risk group, while Pyrimethamine, Axitinib, and Rapamycin may be more beneficial for high-risk patients. In summary, we identified a 6-gene signature related to dendritic cell dysfunction that can predict prognosis in esophageal cancer, offering valuable insights for personalized therapeutic strategies.

P3, N=494, Active, not recruiting, Hangzhou Zhongmei Huadong Pharmaceutical Co., Ltd.

In vivo, metformin inhibited tumor growth, which was negated by RBMS3 silencing. Our findings suggest that metformin promotes ferroptosis and inhibits ovarian cancer progression by upregulating RBMS3, offering a promising direction for clinical application in ovarian cancer treatment.

P=N/A, N=1600, Recruiting, Duke University | Trial completion date: Jul 2026 --> Jul 2027 | Trial primary completion date: Sep 2024 --> Jul 2026

P4, N=96, Recruiting, Bahria University | Active, not recruiting --> Recruiting

However, the high glucose metabolism in inflammatory lesions, driven by macrophage activation, aggregation, and the release of inflammatory factors, is a primary source of false-positive results in FDG PET/CT oncology. This significantly diminishes the specificity and accuracy of PET/CT in diagnosing and staging lung cancer.Here we show FoxO1 plays a role in glucose metabolism in macrophages.We found that metformin regulated FoxO1 expression in macrophages, regulated the expression of inflammatory mediators and apoptosis of macrophages, thus reducing inflammatory glucose metabolism and improving the diagnostic accuracy of 18F-FDG PET/CT in lung cancer.We anticipate that our study could provide a credible approach to improve tumor diagnostic accuracy with PET/CT.

These findings suggest that of HA-Se@CPT, Met, and GW280264X may inhibit tumor progression in BC by improving the function and infiltration of CD8+ T cells. Their effect is more pronounced when used in combination.

P4, N=20, Recruiting, University of Virginia | Not yet recruiting --> Recruiting

P1/2, N=85, Recruiting, Minia University | Not yet recruiting --> Recruiting

P1, N=22, Recruiting, UCB BIOSCIENCES, Inc. | Not yet recruiting --> Recruiting

This study emphasizes the importance of personalized approaches in the use of MAL-PDT, tailoring treatment according to tumor-specific characteristics. Biomarkers such as p53, β-catenin, and GLUT1 can serve as predictive tools for PDT response, helping clinicians identify patients who may benefit from alternative or combined treatments to enhance therapeutic efficacy.

Additionally, metformin reversed the irradiation-induced reduction in the abundance of Lactobacillus and Lachnospiraceae at the genus level. Our findings indicated that metformin ameliorates RILF by downregulating the inflammatory-related HMGB1/TLR4/NF-κB pathway and improving intestinal flora disorder.

We established an in vivo POCD model using isoflurane inhalation anesthesia with exploratory laparotomy...Finally, the PI3K inhibitor, LY294002, reversed the effects of metformin on the levels of PI3K, AKT phosphorylation, and BDNF in vitro cultured HT-22 cells...These results reveal that metformin may alleviate POCD by modulating the PI3K/AKT/BDNF axis. Our study may provide a novel strategy for preventing and treating POCD with this medication.

P1/2, N=85, Not yet recruiting, Minia University

These data reveal early-postmenopause as a critical window when metformin decreases progression of existing disease and highlights the importance of maintaining treatment to prevent metabolic dysregulation, which could promote secondary tumors/metastasis. These findings also help explain the disconnect between epidemiological studies reporting anticancer benefits of metformin and more recent clinical trials that failed to see similar efficacy, potentially due to issues of timing and/or inclusion of women outside the early postmenopausal window and/or without underlying metabolic dysfunction.

P3, N=270, Active, not recruiting, Novo Nordisk A/S | Recruiting --> Active, not recruiting

Mechanistically, the co-treatment with drugs-loaded Cs NPs was found to downregulate the expression of NOTCH-1 and HIF-1α, two key transcription factors involved in tumor cell survival and adaptation, suggesting that their inhibition is a crucial component of the therapeutic efficacy of this treatment strategy. Collectively, the findings of this study suggest that the co-delivery of Met and Dig via chitosan Cs NPs represents a promising therapeutic strategy for breast cancer, as it effectively targets key pathways involved in tumor growth and progression, and underscores the potential of Cs NPs as a versatile platform for cancer therapy.

P=N/A, N=92, Not yet recruiting, RenJi Hospital

P3, N=537, Recruiting, BrightGene Bio-Medical Technology Co., Ltd.

In conclusion, this study provides new insights into the involvement of MetF in ionic interactions with VDAC1, contributing to its anticancer effects in HCC. These findings help elucidate the diverse biological and pharmacological effects of MetF, particularly its influence on autophagy, as well as the potential of MetF as a therapeutic agent for diseases characterized by VDAC1 overexpression.

Presenilin enhancer gamma-secretase subunit (PSENEN), the straight target of metformin, is highly expressed in several cancers...PSENEN may be involved in regulating the immune microenvironment of KIRC, and oxidative phosphorylation may also be a pathway for its involvement in cancer development. PSENEN is a novel prognostic marker for KIRC.

P=N/A, N=70, Not yet recruiting, University of Health Sciences Lahore

Metformin combined with MA may provide an effective option for fertility-sparing treatment of AEH and grade 1 stage IA EAC, and the clinical benefits of metformin for controlling MA-induced weight gain and promoting endometrial expressions of IGFBP-rP1 and p-AMPK while inhibiting p-Akt expression warrants further study.

The study investigated qBOLD imaging's accuracy in identifying hypoxia status within glioblastoma. qBOLD effectively assesses hypoxia and its dynamic evolution in glioblastoma. qBOLD parameters assist in identifying a suitable patient demographic for metformin treatment.

P3, N=840, Recruiting, Fujian Shengdi Pharmaceutical Co., Ltd. | Trial completion date: Mar 2026 --> Sep 2026 | Trial primary completion date: Mar 2026 --> Sep 2026

In vivo experiments using CRC-bearing mouse models, the results confirmed the anti-tumor efficacy of the COMB, leading to substantial inhibition of tumor growth without inducing general toxicity. In conclusion, our study suggests that combining CUR with MET holds promise as a potential option for CRC treatment, with critical mechanisms likely involving ROS elevation, autophagy, and ferroptosis.

Met exerted inhibitory effects on PC through the miR-378a-3p/VEGFA/RGC-32 pathway. Strategies targeting the miR-378a-3p/VEGFA/RGC-32 axis represent a novel avenue for the prevention and treatment of PC.

Metformin inhibited colorectal tumorigenesis by suppressing the TLR4/MyD88/NFκB/MAPK pathway, modulating macrophage M2 polarization and increasing SCFA levels. It holds promise as a potentially effective treatment for colorectal cancer.

In individuals with prediabetes and well-controlled T2D, carnosine supplementation did not result in any significant changes in inflammatory markers. Larger RCTs with longer follow-up durations are needed to evaluate whether carnosine may be beneficial in individuals with poorly controlled T2D.

Thereafter, the pre-diabetic animals were sub-divided into five groups (n = 6), where they were either orally treated with GTIN (15 mg/kg) or metformin (MET) (500 mg/kg), both in the presence and absence of dietary intervention for 12 weeks...These findings may suggest that GTIN administration in both the presence and absence of dietary intervention may offer therapeutic potential in ameliorating cardiovascular disturbances associated with the PD state. However, future studies are needed to determine the physiological mechanisms by which GTIN improves cardiovascular function in the PD state.

Ovarian cancer (OC) remains one of the leading causes of cancer-related mortality among women. Statistical analyses were performed using ordinary one-way or two-way ANOVA, followed by Tukey's or Šídák's multiple comparison tests. While linsitinib shows promise as a therapeutic option for OC, further research is needed to identify agents that could synergize with it to enhance its therapeutic efficacy, like the combination with standard chemotherapy in OC (carboplatin and paclitaxel).

P1, N=14, Active, not recruiting, Boehringer Ingelheim | Recruiting --> Active, not recruiting

P3, N=60, Completed, Tanta University | Recruiting --> Completed | Trial completion date: Oct 2023 --> Jun 2024 | Trial primary completion date: Oct 2023 --> Jun 2024

P1, N=14, Recruiting, Boehringer Ingelheim | Not yet recruiting --> Recruiting