CCG-100602 aids in preventing fibrosis around the temporomandibular joint (TMJ).[1]
CCG-100602 is a CCG-1423 analog with significantly less cytotoxicity (0/14% WST-1 inhibition by 10/100 μM CCG-100602 vs. 44% by 10 μM CCG-1423) and similar efficacy against Rho/MKL1/SRF pathway-mediated transcription (by 78% with 100 μM CCG-100602 vs. 74% with 10 μM CCG-1423; IC50 = 9.8 μM/CCG-100602 vs. 1.5 μM/CCG-1423; by PC-3 SRE-luciferase assay), albeit at a reduced potency. CCG-100602 reduces the stiffening of spontaneously hypertensive rats (SHR) derived aortic VSMCs (1.12 μM) by inhibiting SRF/myocardin interaction and abrogates the increased aortic wall stiffness in SHR rats in vivo (7.5 mg/kg/d via s.c. osmotic pumps for 2 wks).
CCG-1423 analog with similar efficacy and much less cytotoxicity. Inhibits SRF/myocardin interaction and reduces aortic VSMCs stiffening in vitro and in vivo.
Code de la classe de stockage
11 - Combustible Solids
Classe de danger pour l'eau (WGK)
WGK 3
Point d'éclair (°F)
Not applicable
Point d'éclair (°C)
Not applicable
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We recently identified bis(amide) CCG-1423 (1) as a novel inhibitor of RhoA/C-mediated gene transcription that is capable of inhibiting invasion of PC-3 prostate cancer cells in a Matrigel model of metastasis. An initial structure-activity relationship study focusing on bioisosteric replacement
Increased aortic stiffness is a fundamental manifestation of hypertension. However, the molecular mechanisms involved remain largely unknown. We tested the hypothesis that abnormal intrinsic vascular smooth muscle cell (VSMC) mechanical properties in large arteries, but not in distal arteries, contribute
HIV-1 hijacks host cell machinery to ensure successful replication, including cytoskeletal components for intracellular trafficking, nucleoproteins for pre-integration complex import, and the ESCRT pathway for assembly and budding. It is widely appreciated that cellular post-translational modifications (PTMs) regulate protein activity
American journal of respiratory cell and molecular biology, 58(2), 208-215 (2017-09-09)
Radiation-induced pulmonary fibrosis is a severe complication of patients treated with thoracic irradiation. We have previously shown that syndecan-2 reduces fibrosis by exerting alveolar epithelial cytoprotective effects. Here, we investigate whether syndecan-2 attenuates radiation-induced pulmonary fibrosis by inhibiting fibroblast activation.
International journal of molecular medicine, 39(4), 799-808 (2017-03-06)
Malocclusion caused by abnormal jaw development or muscle overuse during mastication results in abnormal mechanical stress to the tissues surrounding the temporomandibular joint (TMJ). Excessive mechanical stress against soft and hard tissues around the TMJ is involved in the pathogenesis
Notre équipe de scientifiques dispose d'une expérience dans tous les secteurs de la recherche, notamment en sciences de la vie, science des matériaux, synthèse chimique, chromatographie, analyse et dans de nombreux autres domaines..
