A dual CCR2/CCR5 chemokine antagonist, BMS-813160?

Norman, Peter

doi:10.1517/13543776.2011.622750

Cited by 22 publications

(10 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As in a previous report, our results demonstrated that both CCR2 and CCR5 are expressed in ATMs of diet‐induced obesity mice (Figure ). In this background, novel agents that simultaneously antagonize multiple chemokine receptors, such as dual CCR2/CCR5 antagonists, have been developed . However, to date, there have been few studies investigating the effect of a dual chemokine receptor antagonist on obesity‐related chronic metabolic disease.…”

Section: Discussionmentioning

confidence: 99%

Dual CCR2/5 Antagonist Attenuates Obesity‐Induced Insulin Resistance by Regulating Macrophage Recruitment and M1/M2 Status

Huh

Kim

Lee

et al. 2017

Obesity

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Dual CCR2/5 Antagonist Attenuates Obesity‐Induced Insulin Resistance by Regulating Macrophage Recruitment and M1/M2 Status

Huh

Kim

Lee

et al. 2017

Obesity

View full text Add to dashboard Cite

show abstract

“…CCR5 blockade led to clinical responses in colorectal cancer patients,w ith regression of metastases and changes in the tumor microenvironment without significant side effects. [83,84] Moreover,aphase I/II study of ad ual CCR2/5 antagonist BMS-813160 (structure not disclosed, BMS) [85] in combination with nivolumab for patients with advanced solid tumors is envisaged to start in 2017. [86]…”

Section: Angewandte Chemiementioning

confidence: 99%

Small Molecules Drive Big Improvements in Immuno‐Oncology Therapies

2018

View full text Add to dashboard Cite

Immuno‐oncology therapies have the potential to revolutionize the armamentarium of available cancer treatments. To further improve clinical response rates, researchers are looking for novel combination regimens, with checkpoint blockade being used as a backbone of the treatment. This Review highlights the significance of small molecules in this approach, which holds promise to provide increased benefit to cancer patients.

show abstract

“…inhibitor [36], and Stattic, STAT3 inhibitor [37], were also used to estimate the potential therapeutic effect. It found that compared with AT3 cells alone, combined injection of mature 3T3-L1 accelerated the tumor growth of xenografts (P < 0.05; Fig.…”

Section: Macrophages De Ciency In Tumor-adipocyte Interaction Inhibitmentioning

confidence: 99%

Macrophages in Tumor-Associated Adipose Microenvironment Accelerate Tumor progression

Yang

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Macrophages particularly contribute to the progression of obesity-related tumor. However, the mechanisms that the tumor-adipocyte crosstalk may enable the properties and plasticity of macrophages remain still unclear. Methods: Survival probabilities for recurrence-free survival (RFS) were estimated by the Kaplan–Meier method based on immunohistochemistry and immunofluorescence images. 3T3-L1 cells were co-cultivated with 4T1 and MDA-MB-231 cells. Then the co-cultivated media were used to treat THP-1/RAW264.7 cells. The markers of macrophages were detected by immunofluorescence and Western blot. Transwell migration assay, was conducted to determine the migration capability of macrophages. RT-PCR and ELISA were used to detect the expression and secretion level of chemokines, respectively. Immunofluorescence imaging and Western blot were used to investigate the role of SOCS6/STAT3 signaling pathway in the polarization of macrophages. microRNA mimic and inhibitor, and xenograft models were used to explore the role of miR-155 in the polarization of macrophages.Results: We demonstrate that CD163-positive macrophages aggregated to surround adipocytes in breast cancer tissues, which was associated with tumor relapse. In tumor-adipocyte microenvironment, CD163-positive macrophages are recruited and polarized via the elevated expression of CCL2 and CCL5. Consistently, the eliminated macrophages partially inhibited adipocytes-induced tumor proliferation. Likewise, inhibiting chemokines and their receptors or suppressing the phosphorylation of STAT3 significantly decreased tumor burden in vivo. Finally, the source of CCL2 and CCL5 mainly derived from adipocytes. In coculture of tumor cells and adipocytes, the level of exosomal miRNA-155 was high, then it promoted the generation and release of CCL2 and CCL5 from adipocytes through targeting SOCS6/STAT3 pathway. Inhibition of exosomal miRNA-155 in tumor cells reduced the CCL2 and CCL5 levels in tumor-adipocytes coculture, and further retarded tumor growth. Conclusion: These results suggest a novel target of tumor-adipocyte-macrophage interconnect that could facilitate obesity-induced tumor progression.

show abstract

A dual CCR2/CCR5 chemokine antagonist, BMS-813160?

Cited by 22 publications

References 10 publications

Dual CCR2/5 Antagonist Attenuates Obesity‐Induced Insulin Resistance by Regulating Macrophage Recruitment and M1/M2 Status

Dual CCR2/5 Antagonist Attenuates Obesity‐Induced Insulin Resistance by Regulating Macrophage Recruitment and M1/M2 Status

Small Molecules Drive Big Improvements in Immuno‐Oncology Therapies

Macrophages in Tumor-Associated Adipose Microenvironment Accelerate Tumor progression

Contact Info

Product

Resources

About