Kartogenin (KGN)

  Cat. No.:  DC7669   Featured
Chemical Structure
4727-31-5
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Field of application
Kartogenin(KGN) is a small molecule stimulator of chondrogenesis; promotes chondrocyte differentiation(EC50=100 nM) and binds to filamin A.
Cas No.: 4727-31-5
Chemical Name: 2-([1,1'-Biphenyl]-4-ylcarbamoyl)benzoic acid
Synonyms: 2-([1,1'-Biphenyl]-4-ylcarbamoyl)benzoic acid;Kartogenin;2-?[(Biphenyl-?4-?yl)?carbamoyl]?benzoic acid;2-[([1,1'-Biphenyl]-4-ylaMino)carbonyl]benzoic Acid;KGN;2-(biphenyl-4-ylcarbamoyl)benzoic acid;AC1MCUNV;CBDivE_009769;Maybridge3_004725;Oprea1_848730;SureCN1336628;2-[(Biphenyl-4-yl)carbamoyl]benzoic acid;4′-Phenyl-phthalanilic acid (8CI)
SMILES: O=C(O)C1=CC=CC=C1C(NC2=CC=C(C3=CC=CC=C3)C=C2)=O
Formula: C20H15NO3
M.Wt: 317.338
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: Kartogenin is an inducer of differentiation of human mesenchymal stem cells into chondrocytes.
In Vivo: hen injected into intact rat patellar tendons, kartogenin induces cartilage-like tissue formation in the injected area. When injected into experimentally injured rat Achilles TBJs, wound healing in the TBJs is enhanced, as evidenced by the formation of extensive cartilage-like tissues[1]. Kartogenin stimulates collagen synthesis in the mouse dermis. Dermis in the kartogenin (100 nM)-treated group exhibits increased dermal thickness and intense blue staining, which represents more collagen composition in the dermis[2].
In Vitro: Kartogenin enhances cell proliferation in both cell types in a concentration-dependent manner and induces chondrogenic differentiation of stem cells, as demonstrated by high expression levels of chondrogenic markers aggrecan, collagen II and Sox-9. Besides, kartogenin induces the formation of cartilage-like tissues in cell cultures, as observed through the staining of abundant proteoglycans, collagen II and osteocalcin[1]. Kartogenin stimulates type-I collagen synthesis of fibroblasts at the mRNA and protein levels in a time-dependent manner without obvious influence on fibroblasts’ apoptosis and viability. Smad4/smad5 of the TGF-β signaling pathway is activated by kartogenin while MAPK signaling pathway remains unchanged[2]. Kartogenin treatment enhances chondrocyte pericellular matrix assembly and retention in the presence of IL-1β. Kartogenin partially blocks the IL-1β-induced increased expression of ADAMTS-5. Additionally, kartogenin-treated articular chondrocytes exhibits a decrease in CD44 proteolytic fragmentation[3].
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
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