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| Cat. No. : | HY-117843 |
| M.Wt: | 355.43 |
| Formula: | C21H25NO4 |
| Purity: | >98 % |
| Solubility: | 10 mM in DMSO |
Ppc-1 is a mitochondrial uncoupler. Ppc-1 enhances mitochondrial oxygen consumption without adverse effects on ATP production. Ppc-1 is a cell-permeate interleukin-2 (IL-2) inhibitor. Ppc-1 inhibits the Gram-negative periodontopathogen Porphyromonas gingivalis. Ppc-1 has anti-obesity, antibacterial and anti-inflammatory activities[1][2][3][4].
IC50 & Target: Mitochondrial[1]
Interleukin-2 (IL-2)[2]
Porphyromonas gingivalis[4]
In Vitro: Ppc-1 treatment (0-10 μM; 24 hours; Jurkat cells) significant inhibits IL-2 production in Jurkat cells with an IC50 of 4 μM[2].
Ppc-1 (compound 6) has antiproliferative activities in K562 human leukemia, Hela cervical carcinoma, and 3T3-L1 mouse embryonic fibroblast cells. Ppc-1 shows about 50% inhibition at 15 μM in all cell lines. Ppc-1 inhibits the growth of K562 cells with an EC50 of 13 μM[3].
Using the U937-3xκB-LUC human monocytic cell line, Ppc-1 dose-dependently inhibits the lipopolysaccharide-induced NF-κB activation[4].
In Vivo: Ppc-1 (0-10 mg /kg; Intraperitoneal injection; once a week; for 8 weeks; female ICR mice) treatment suppresses weight gain with no abnormal effects on liver or kidney tissues, and no evidence of tumor formation[1].
Serum fatty acid levels are significantly elevated in mice treated with Ppc-1, while body fat content remained low. After a single administration, Ppc-1 distributes into various tissues of individual animals at low levels. Ppc-1 stimulates adipocytes in culture to release fatty acids, which might explain the elevated serum fatty acids in Ppc-1-treated mice[1].
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