tfm

TFM is a piscicide.1It is toxic to sea lamprey (P. marinus) with LC50values ranging from 1.97 to 2.11 and 2.05 to 2.21 mg/L for sac and swim-up fry, respectively, 1.6 to 2.45 mg/L for juveniles, and 1.6 to 1.63 mg/L for adults. It is also toxic to juvenile lake sturgeon (A. fulvescens) less than 100 mm in size but not to a variety of other fish species. TFM (50 μM) uncouples oxidative phosphorylation by 22 and 28% in isolated sea lamprey and rainbow trout (O. mykiss) liver, respectively.2Formulations containing TFM have been used as lampricides in the control of larval sea lamprey populations. 1.Boogaard, M.A., Bills, T.D., and Johnson, D.A.Acute toxicity of TFM and a TFM/niclosamide mixture to selected species of fish, including lake sturgeon (Acipenser fulvescens) and mudpuppies (Necturus maculosus), in laboratory and field exposuresJ. Great Lakes Res.29(Suppl 1)529-541(2003) 2.Birceanu, O., McClelland, G.B., Wang, Y.S., et al.The lampricide 3-trifluoromethyl-4-nitrophenol (TFM) uncouples mitochondrial oxidative phosphorylation in both sea lamprey (Petromyzon marinus) and TFM-tolerant rainbow trout (Oncorhynchus mykiss)Comp. Biochem. Physiol. C. Toxicol. Pharmacol.153(3)342-349(2011)

844-TFM is an NBTI (novel bacterial topoisomerase inhibitor) DNA gyrase inhibitor (IC50: 1.5 μM). 844-TFM exhibits bactericidal activity against Mycobacterium abscessus.

androgen receptor modulator

TFMU-ADPr triethylamine, a versatile substrate for evaluating poly(ADP-ribose) glycohydrolase (PARG) activity, enables direct measurement of total PAR hydrolase activity through the liberation of a fluorophore. With outstanding reactivity, generality, stability, and usability, it serves as an essential tool for the in vitro assessment of small-molecule inhibitors and exploration of the regulation of ADP-ribosyl catabolic enzymes [1].

TFMB-(S)-2-HG (TFMB S 2 HG) is a highly effective inhibitor of TET2, the 5'-methylcytosine hydroxylase. Additionally, it significantly inhibits the EglN prolyl hydroxylases. With its unique properties, TFMB-(S)-2-HG holds great promise for advancing research in the field of acute myeloid leukemia (AML).

TFMB-(R)-2-HG is a cell membrane-permeable (R)-2-HG, an oncogenic factor in acute myeloid leukemia. It impairs SCF ER-Hoxb8 cell differentiation in response to estrogen withdrawal.