Teleocidin A1, also known as lyngbyatoxin A, is a fungal metabolite that has been isolated from S. mediocidicus and is the R enantiomer of (S)-teleocidin A. [1] It acts as a tumor promoter, inducing ornithine decarboxylase activity in mouse skin, increasing adhesion of HL-60 human leukemia cells (ED50 = 7 ng/ml), and inducing tumor formation in 87% of mice after 30 weeks when administered at a dose of 3 &#181g twice per week. [2] Teleocidin A1 also increases the production of prostaglandins and the turnover of choline in HeLa cells when used at concentrations ranging from 6 to 20 ng/ml. [3] It is a substrate for the methyltransferase TleD in Streptomyces where it is converted to teleocidin B.[4]

Reference:
[1]. Sakai, S.-I., Hitotsuyanagi, Y., Aimi, N., et al. Absolute configuration of lyngbyatoxin A (teleocidin A-1) and teleocidin A-2. Tetrahedron Lett. 27(43), 5219-5220 (1986).
[2]. Fujiki, H., and Sugimura, T. New classes of tumor promoters: Teleocidin, aplysiatoxin, and palytoxin. Adv. Cancer Res. 49, 223-264 (1987).
[3]. Sakamoto, H., Terada, M., Fujiki, H., et al. Stimulation of prostaglandin production and choline turnover in HeLa cells by lyngbyatoxin A and dihydroteleocidin B. Biochem. Biophys. Res. Commun. 102(1), 100-107 (1981).
[4]. Yu, F., Li, M., Xu, C., et al. Crystal structure and enantioselectivity of terpene cyclization in SAM-dependent methyltransferase TleD. Biochem. J. 473(23), 4385-4397 (2016).