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PH 797804

an NSAID; structure in first source

Also Known As:

PH-797804; PH797804

Networked: 10 relevant articles (2 outcomes, 2 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1.	Aldovini, Anna: 1 article (01/2018)
2.	Allémann, Eric: 1 article (01/2018)
3.	Chaudhary, Omkar: 1 article (01/2018)
4.	Hashem, Hanaa Ma: 1 article (01/2018)
5.	Jordan, Olivier: 1 article (01/2018)
6.	Lelis, Felipe: 1 article (01/2018)
7.	Linz, Brandon: 1 article (01/2018)
8.	Mahrouse, Marianne A: 1 article (01/2018)
9.	Maudens, Pierre: 1 article (01/2018)
10.	Narayan, Vivek: 1 article (01/2018)

Related Diseases

1.	Infections 01/01/2018 - "Importantly, the addition of PH-797804 to ART initiated during chronic SIV infection reduced immune activation and restored immune system parameters to the levels observed when ART was initiated on week 1 after infection. " 01/01/2018 - "We concluded that the inhibitor PH-797804 significantly reduced, even if did not normalized, the immune activation parameters evaluated during ART treatment, improved preservation of critical populations of the immune system targeted by SIV, and increased the efficacy of ART treatment initiated in chronic infection to levels similar to those observed when initiated in acute infection but did not affect positively or negatively viral reservoirs." 01/01/2023 - "Using primary human lung explants and lung epithelial organoids, we demonstrate that targeting p38 signal transduction with the selective and clinically pre-evaluated inhibitors PH-797804 and VX-702 markedly reduced the expression of the pro-inflammatory cytokines IL6, CXCL8, CXCL10 and TNF-α during infection, while viral replication and the interferon-mediated antiviral response of the lung epithelial barrier were largely maintained. "
2.	Fibrosis (Cirrhosis) 11/01/2017 - "In mice, PH797804 improved RV function and inhibited cardiac fibrosis compared with placebo. "
3.	Persistent Infection 01/01/2018 - "We concluded that the inhibitor PH-797804 significantly reduced, even if did not normalized, the immune activation parameters evaluated during ART treatment, improved preservation of critical populations of the immune system targeted by SIV, and increased the efficacy of ART treatment initiated in chronic infection to levels similar to those observed when initiated in acute infection but did not affect positively or negatively viral reservoirs."
4.	Inflammation (Inflammations) 10/01/2015 - "PH-797804 had the greatest impact on neutrophilic airway inflammation. " 01/01/2018 - "Metabolism study of PH-797804, a promising newly developed drug for treatment of chronic inflammation which inhibits P38 mitogen-activated protein kinase. " 12/01/2009 - "Furthermore, PH-797804 demonstrates robust anti-inflammatory activity in chronic disease models, significantly reducing both joint inflammation and associated bone loss in streptococcal cell wall-induced arthritis in rats and mouse collagen-induced arthritis. " 12/01/2009 - "PH-797804 is an ATP-competitive, readily reversible inhibitor of the alpha isoform of human p38 MAP kinase, exhibiting a K(i) = 5.8 nM. In human monocyte and synovial fibroblast cell systems, PH-797804 blocks inflammation-induced production of cytokines and proinflammatory mediators, such as prostaglandin E(2), at concentrations that parallel inhibition of cell-associated p38 MAP kinase. "
5.	Osteoarthritis 01/01/2018 - "This study aimed to formulate nanocrystal-polymer particles (NPPs) containing the potent p38α/β MAPK inhibitor PH-797804 (PH-NPPs) and to test their extended-release properties over months in comparison to those of conventional PH microparticles for the intra-articular treatment of inflammatory and mechanistic murine models mirroring aspects of human osteoarthritis (OA). "

Related Drugs and Biologics

1.	p38 Mitogen-Activated Protein Kinases
2.	Polymers
3.	N-(3-pyridyl)-3-phenylsuccinimide
4.	Cytokines
5.	Antiviral Agents (Antivirals)
6.	Protein Isoforms (Isoforms)
7.	Interleukin-6 (Interleukin 6)
8.	Prostaglandins
9.	Interferons
10.	Adenosine Triphosphate (ATP)