CAS 153190-29-5 U-74389G - Analytical Products / Alfa Chemistry

CAT	AP153190295
CAS	153190-29-5
MDL Number	MFCD01074991
Molecular Weight	726.90
InChI Key	ABCSSKWSUJMJCP-WQDFMEOSSA-N

Solubility	ethanol: soluble 20 mg/mL, clear, light yellow
Size	100MG
Storage Conditions	−20°C

Lazaroid U-74389G Administration in Pancreatic Ischemia-Reperfusion Injury: A Swine Model Encompassing Ischemic Preconditioning

Dimosthenis T Chrysikos, Theodoros N Sergentanis, Flora Zagouri, Theodora Psaltopoulou, George Theodoropoulos, Ioannis Flessas, George Agrogiannis, Nikolaos Alexakis, Maria Lymperi, Ageliki I Katsarou, etc.

JOP. 2015 Mar 20;16(2):176-84.

PMID: 25791552

Lazaroid U-74389G for Cardioplegia-Related Ischemia-Reperfusion Injury: An Experimental Study

Panagiotis Dedeilias, Apostolos Papalois, Christos Angelidis, Georgios Giannopoulos, Spyridon Deftereos, Maria Chorti, Efstratios Apostolakis, Georgia Kostopanagiotou

J Surg Res. 2017 Jan;207:164-173.

PMID: 27979473

Lazaroid U-74389G in Liver Ischemia-Reperfusion Injury: A Swine Model

Maria I Korontzi, George Theodoropoulos, George Agrogiannis, Ioannis Flessas, Dimosthenis Chrysikos, Aristea Gioxari, Theodoros N Sergentanis, Efstratios Patsouris, George C Zografos, Apostolos Papalois

Exp Ther Med. 2019 Jul;18(1):230-236.

PMID: 31258658

The Effect of the Antioxidant Drug "U-74389G" on Oophoritis During Ischemia Reperfusion Injury in Rats

Constantinos Τsompos, Constantinos Panoulis, Konstantinos Tauοutouzas, George Zetaografos, Apostolos Papalois

Antiinflamm Antiallergy Agents Med Chem. 2014;13(2):103-7.

PMID: 25091819

The Effect of U-74389G on Pancreas Ischemia-Reperfusion Injury in a Swine Model

Dimosthenis T Chrysikos, Theodoros N Sergentanis, Flora Zagouri, Theodora Psaltopoulou, Ioannis Flessas, George Agrogiannis, Nikolaos Alexakis, Ioannis Bramis, Evgenia E Patsouri, Efstratios S Patsouris, etc.

J Surg Res. 2014 Apr;187(2):450-7.

PMID: 24332939

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Case Study

Lazaroid U-74389G Inhibits Osteogenic Differentiation of IL-1β-Induced Aortic Valve Interstitial Cells

Sun, Fuqiang, et al. The Journal of Steroid Biochemistry and Molecular Biology 152 (2015): 114-123.

Aortic valve calcification is described as an active process involving aortic valve interstitial cells (AVIC) and is considered an inflammatory disease. As an antioxidant, the anti-inflammatory activity of Lazaroid has been demonstrated in various models. This study hypothesizes that Lazaroid U-74389G would inhibit the osteogenic differentiation of IL-1β-induced AVIC.
Normal trileaflet aortic valve leaflets were collected from patients undergoing Bentall surgery for acute aortic dissection (Type A). AVIC were isolated in culture and stimulated with IL-1β in the presence or absence of U-74389G. Osteogenic markers and nuclear factor-κB (NF-κB) were analyzed in cell lysates using real-time PCR and Western blotting. IL-6 and IL-8 levels in the culture medium were measured using ELISA. Alizarin red staining was used to visualize calcium deposition.
The expression of alkaline phosphatase and bone morphogenetic proteins was upregulated under IL-1β stimulation, along with the production of IL-6 and IL-8, while the addition of U-74389G inhibited this expression. The NF-κB pathway was activated by IL-1β and contributed to the inhibition of osteogenic differentiation in AVIC by U-74389G. The glucocorticoid receptor antagonist mifepristone and the NF-κB inhibitor Bay 11-7082 were able to block the negative effects of U-74389G on the expression of osteogenic genes and mineralization in AVIC.

Pharmacological Inhibition of Lipid Peroxidation Damage by 21-Aminosteroid U-74389G

Hill, Rachel L., et al. Neuropharmacology 170 (2020): 108023.

21-aminosteroid ("lazaroid") U-74389G (U74) is a lipid peroxidation (LP) inhibitor used to protect mitochondrial function after traumatic brain injury (TBI) in adult male mice.
These animals underwent severe (2.2 mm) controlled cortical impact-TBI. U74 was intravenously administered at 15 minutes and 2 hours post-injury (hpi), followed by intraperitoneal injection of the following doses (mg/kg) at 8 hpi: 0.3 (IV) + 1 (IP), 1 + 3, 3 + 10, and 10 + 30. Total cortical mitochondria were isolated at 72 hpi, and respiration rates were measured. Mitochondrial 4-HNE and acrolein were evaluated as indicators of LP-mediated oxidative damage.
Compared to sham-operated animals, the mitochondrial respiration rate was significantly reduced in injured animals at 72 hours post-TBI. Administration of U74 at a dose of 1 mg/kg significantly improved the mitochondrial respiration rates of states II, III, and V(II), as well as the respiratory control ratio (RCR), compared to animals receiving vehicle treatment. Additionally, administration of U74 reduced levels of reactive aldehydes in injured animals at 72 hours post-TBI compared to those receiving vehicle treatment.