Catalog No.S1314 Synonyms: Zoledronate, CGP-4244
Molecular Weight(MW): 272.09
Zoledronic acid (ZA), a potent osteoclast inhibitor, induces apoptosis in osteoclasts by inhibiting enzymes of the mevalonate pathway and preventing the isoprenylation of small GTP-binding proteins such as Ras and Rho.
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Quantification (C) of SA-β-gal+ SMCs after sustained 100nM ADP treatment for 48hr with or without Ras inhibitor zoledronic acid (ZA) (n=4 in each group). #p<0.05, ##p<0.01 compared with control, *p<0.05 compared with P2ry12+/+ADP. (D) Incidence of TAAD formation and rupture after BAPN administration with or without ZA. (E) Elastin degradation grades of mice aortas after BAPN administration with or without ZA. (F) Representative H&E staining of thoracic aorta and progression of thoracic aorta diameter of mice aortas after BAPN administration with or without ZA (n=8 in both group). (G) Representative images and quantification of SA-β-gal (blue) staining in mouse aorta after BAPN administration with or without ZA (n=4 in both group); arrow, location of SA-β-gal+ area. (H) Immunostaining and quantification of p-ERK and p-p38 in mouse aorta with or without ZA (n=4 in both group). Data are meanSD from three experiments.*p<0.05, compared with no ZA.
J Mol Cell Cardiol, 2016, 99:76-86.. Zoledronic Acid purchased from Selleck.
Isolation of cd T cells. PBMCs were cultured in the presence of 400 nM ZA and 200 IU/ml IL-2 over 10 days. cd T cells were isolated by negative MACS isolation. Flow cytometric analysis revealed co-expression of CD3 and TCRcd on over 99% of cells of the flow through fraction (A). The T cells expressed the TCRVd2 chain (B) and the CD56 protein (C).
Liver Int 2013 33(1), 127-36. Zoledronic Acid purchased from Selleck.
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|Description||Zoledronic acid (ZA), a potent osteoclast inhibitor, induces apoptosis in osteoclasts by inhibiting enzymes of the mevalonate pathway and preventing the isoprenylation of small GTP-binding proteins such as Ras and Rho.|
Zoledronic acid (10 µM and 100 µM) causes a significant reduction in the proportions of MCF-7 cells (49.54% and 23.55% of control, respectively) (P < 0.05). Zoledronic acid has little effect on MDA-MB-231 cells at concentrations of 0.1–10 µM, whereas the 100 µM concentration results in a significant reduction in cell number. Zoledronic acid (100 µM) results in a 63.5% reduction in MCF-7 cell number at 72 hours and an 87.1% reduction at 96 hours. Zoledronic acid (10 µM) results in a greater than 4-fold increase in MCF-7 cell apoptosis whereas the 100 µM concentration induces a 6-fold increase in the proportion of apoptotic cells. Zoledronic acid (10 µM) and paclitaxel (2 µM) results in a 5-fold increase in apoptosis (774.8% of control) compared to zoledronic acid alone (155.71%) and a 4-fold increase compared to paclitaxel alone (189.68%). Zoledronic acid-induced apoptosis of MCF-7 breast cancer cells can be inhibited by addition of intermediates of the mevalonate pathway, which is consistent with observations in osteoclasts, macrophages and myeloma cells.  Zoledronic acid enhances OPG gene expression and protein secretion by human osteoblasts (hOB) in a dose-dependent fashion with a maximum effect at 10 nM after 72 hours, consistent with the higher biological potency of Zoledronic acid. Zoledronic acid prevents the inhibitory effects of the glucocorticoid dexamethasone on OPG mRNA and protein production in human osteoblasts. Zoledronic acid induces type I collagen secretion and alkaline phosphatase activity by 2- and 4-fold, respectively, in human osteoblasts. 
|In vivo||Zoledronic acid (120 mg/kg, s.c.) prevents the formation of lesions, prevents cancellous bone loss and loss of bone mineral density, and reduces osteoclast perimeter in 5T2MM-bearing mice. Zoledronic acid (120 mg/kg, s.c.) also decreases paraprotein concentration, decreases tumor burden, and reduces angiogenesis in 5T2MM-bearing mice. |
|In vitro||0.1M NaOH (aq)||40 mg/mL (147.01 mM)|
|DMSO||0.004 mg/mL (0.01 mM)|
|In vivo||Add solvents individually and in order:
30% PEG400+0.5% Tween80+5% Propylene glycol
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02632903||Not yet recruiting||Osteoporosis|Osteonecrosis|Acute Lymphoblastic Leukemia||Childrens Hospital of Eastern Ontario||October 2016||Phase 2|
|NCT02721433||Recruiting||Breast Cancer|Prostate Cancer|Metastasis||Ottawa Hospital Research Institute||August 2016||Phase 4|
|NCT02632916||Recruiting||Osteoporosis||Childrens Hospital of Eastern Ontario||August 2016||Phase 2|
|NCT02480634||Not yet recruiting||Non-small Cell Lung Cancer|Bone Metastasis||Daping Hospital and the Research Institute of Surgery of the Third Military Medical University||June 2016||Phase 4|
|NCT02508038||Recruiting||Acute Myeloid Leukemia|Acute Lymphoblastic Leukemia|Hodgkin Lymphoma|Non-Hodgkin Lymphoma|Myelodysplastic Syndrome|Myeloproliferative Syndrome|Rhabdomyosarcoma|Ewing Sarcoma|Primitive Neuroectodermal Tumor|Osteosarcoma|Neuroblastoma||University of Wisconsin, Madison||January 2016||Phase 1|
|NCT02069340||Not yet recruiting||Malignant Neoplasm|Musculoskeletal Complications||University of Southern California|National Cancer Institute (NCI)||January 2016||--|
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