dmc

Se-DMC has antioxidant, anti-damage and anti-edema properties and can be used to study diseases related to metabolism and inflammation.

4-Ethyl-N,N-Dimethylcathinone hydrochloride is an analog of Methedrone, which is a cathinone-related compound. As a non-selective substrate for monoamine transporters, Methedrone promotes the release of neurotransmitters.

DMCM hydrochloride is a non-selective fully inverse agonist of benzodiazepine. DMCM showed significant differences in human recombinant GABAA αxβ3γ2 receptor subtypes. For α1, α2, α3, and α5 receptors, their Kis were 10 nM, 13 nM, 7.5 nM, 2.2 nM, respectively.

dMCL1-2 is a potent and selective myeloid leukemia 1 (MCL1) degrading agent based on PROTAC, binding to MCL1 with a KD of 30 nM and activating the apoptosis mechanism by degrading MCL1.

NDMC101 is an inhibitor of dipeptidyl peptidase-IV activity in human T cells and exhibits immunomodulatory effects. It also acts as a novel inhibitor of NFATc1 and NF-κB activity.

Palmitic acid (Cetylic acid) is a natural product, a common saturated fatty acid found in animals, plants and microorganisms. Palmitic acid has antitumor activity.

XDM-CBP is an effective and selective CBP/p300 bromodomain inhibitor.

Cinnamic acid, m-chloro-alpha-methyl-, 7-nitro-8-quinolyl ester is a bioactive chemical.

DM-CHOC-PEN is a DNA alkylation agent that may be used to treat brain cancer.

(1E,6E)-Bis(demethoxy)curcumin (Curcumin III) is a natural demethoxy derivative of curcumin,with anti-inflammatory and anti-cancer activities.

DM-CO-(CH2)5-SMe, derived from an antibody-drug conjugate (ADC) metabolite, serves as an anticancer agent with demonstrated cytotoxicity against H1703, H1975, COLO704, and Colo720E cells [1].

5,6-DM-cBIMP, a cyclic nucleotide analog, acts as a PDE2 agonist, significantly enhancing the hydrolytic activity of PDE2 on cAMP and cGMP.

Bisdemethoxycurcumin is a natural curcumin derivative that activates the AMPKα pathway to attenuate LPS-induced acute lung injury; reversibly inhibits tyrosinase and possesses anti-browning ability; enhances the antiprostate cancer efficacy of docetaxel (DTX); targets cellular pathways involved in oxidative stress and apoptosis; and is an anticancer agent.

Decarbamoylmitomycin C, an analog of Mitomycin C (MC), functions as a DNA alkylating agent. It is capable of activating chromatin relaxation by the ataxia-telangiectasia and Rad3-related protein (ATR) in a p53-independent manner.

2,5-dimethyl Celecoxib is a derivative of celecoxib that does not inhibit COX-2 (IC50 = >100 μM).1 It does inhibit microsomal prostaglandin E synthase-1 (mPGES-1) in HeLa cells (IC50 = 15.6 μM) and reduces prostaglandin E2 production in HeLa, A549, and HCA-7 cells (IC50s = 0.64, 0.83, and 3.08 μM, respectively).2 It inhibits proliferation of drug-sensitive RPMI8226 and multidrug-resistant 8226/Dox40 multiple myeloma cells, as well as increases the rate of apoptosis when used at concentrations of 20 and 30 μM.3 2,5-dimethyl Celecoxib reduces the expression of survivin, cyclin A, cyclin B, MEK1, and MEK2 in 8226/Dox40 cells. The antiproliferative effect of 2,5-dimethyl celecoxib is independent of mPGES-1 inhibition.2References1. Zhu, J., Song, X., Lin, H.-P., et al. Using cyclooxygenase-2 inhibitors as molecular platforms to develop a new class of apoptosis-inducing agents. J. Natl. Cancer Inst. 94(23), 1745-1757 (2002).2. Wobst, I., Schiffmann, S., Birod, K., et al. Dimethylcelecoxib inhibits prostaglandin E2 production. Biochem. Pharmacol. 76(1), 62-69 (2008).3. Kardosh, A., Soriano, N., Liu, Y.-T., et al. Multitarget inhibition of drug-resistant multiple myeloma cell lines by dimethyl-celecoxib (DMC), a non-COX-2 inhibitory analog of celecoxib. Blood 106(13), 4330-4338 (2005). 2,5-dimethyl Celecoxib is a derivative of celecoxib that does not inhibit COX-2 (IC50 = >100 μM).1 It does inhibit microsomal prostaglandin E synthase-1 (mPGES-1) in HeLa cells (IC50 = 15.6 μM) and reduces prostaglandin E2 production in HeLa, A549, and HCA-7 cells (IC50s = 0.64, 0.83, and 3.08 μM, respectively).2 It inhibits proliferation of drug-sensitive RPMI8226 and multidrug-resistant 8226/Dox40 multiple myeloma cells, as well as increases the rate of apoptosis when used at concentrations of 20 and 30 μM.3 2,5-dimethyl Celecoxib reduces the expression of survivin, cyclin A, cyclin B, MEK1, and MEK2 in 8226/Dox40 cells. The antiproliferative effect of 2,5-dimethyl celecoxib is independent of mPGES-1 inhibition.2 References1. Zhu, J., Song, X., Lin, H.-P., et al. Using cyclooxygenase-2 inhibitors as molecular platforms to develop a new class of apoptosis-inducing agents. J. Natl. Cancer Inst. 94(23), 1745-1757 (2002).2. Wobst, I., Schiffmann, S., Birod, K., et al. Dimethylcelecoxib inhibits prostaglandin E2 production. Biochem. Pharmacol. 76(1), 62-69 (2008).3. Kardosh, A., Soriano, N., Liu, Y.-T., et al. Multitarget inhibition of drug-resistant multiple myeloma cell lines by dimethyl-celecoxib (DMC), a non-COX-2 inhibitory analog of celecoxib. Blood 106(13), 4330-4338 (2005).