Reference

Choline and halogen derivatives of CMA (9-oxo-10-acridineacetic acids) as tools for monitoring the interaction of the interferon inducers via a specific receptor

Choline and halogen derivatives of CMA (9-oxo-10-acridineacetic acids) as tools for monitoring the interaction of the interferon inducers via a specific receptor. Szulc, B.; Szulc, Z.; Inglot, A. D.; Inglot, O.; Mlochowski, J.; Fikus, M.; Albin, M. (Inst. Immunol. Exp. Ther., Pol. Acad. Sci., Wroclaw 53-114, Pol.). Antiviral Res., 7(2), 109-17 (English) 1987. CODEN: ARSRDR. 108119-61-5 and 38609-97-1 are also in the experiment. ISSN: 0166-3542. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) New choline and halogen derivs. of 9-oxo-10-acridineacetic acid (CMA) [38609-97-1] were investigated as interferon (IFN) inducers in mice and in the mouse bone marrow-derived macrophage cultures. Two of the choline derivs., (N,N-dimethylamino)ethyl ester of CMA (I) [108119-58-0] and cholinium 9-oxo-10-acridine acetate (II) [108119-59-1], were active IFN inducers presumably because they were hydrolyzed so as to release CMA. The halogen analogs of CMA were inactive or weak IFN inducers in vivo and in vitro. On the contrary, the Br and I derivs. of CMA were potent inhibitors of IFN induction by CMA in vitro. The behavior of the agonists and antagonists of CMA suggests that the induction of interferon may occur indirectly via a specific CMA-receptor complex. .

Cyclic AMP metabolism and interferon induction in mice after treatment with 10-carboxymethyl-9-acridanone

Cyclic AMP metabolism and interferon induction in mice after treatment with 10-carboxymethyl-9-acridanone. Roemer, W.; Tonew, E.; Schulze, W. (Cent. Inst. Microbiol. Exp. Therapy, Ger. Acad. Sci., Jena 6900, Ger. Dem. Rep.). Acta Virol. (Engl. Ed.), 30(5), 411-17 (English) 1986. CODEN: AVIRA2. ISSN: 0001-723X. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The low mol. wt. substance 10-carboxymethyl-9-acridanone (CMA)(I) [38609-97-1] is capable to induce interferon (IFN) prodn. 38609-97-1 and 60-92-4 are cas registry numbers of chemicals which are used as reagents here. In order to det. the effect of CMA on cAMP [60-92-4] alterations in relation to IFN prodn., male ABD2F1 hybrid mice were orally treated with several concns. of CMA (400, 600 and 800 mg/kg) for varying periods of time up to 24 h. IFN titers were detected as early as 3 and 4 h, resp., in mouse plasma after CMA administration, and their prodn. continued for at least 24 h. Max. IFN titers were assayed in the presence of 800 mg/kg (3 200 IU/mL)CMA. Measuring of the intracellular concns. of cAMP in thymus and spleen revealed that in early stage (3.5-2 h) CMA exhibited a dose-dependent increase. The drug acted as an inhibitor of low Km cAMP phosphodiesterase [9036-21-9] in cell homogenates; a significantly enhanced enzyme activity (1 to 4 h) was found after exposure to CMA in vivo. .