Synonym: (3R)-Anthracen-9-yl-[3-(morpholine-4-carbonyl)-[1,4′]bipiperidinyl-1′-yl]-methanone hydrochloride; CP 640186 hydrochloride; CP640186 hydrochloride; [(3R)-1′-(9-Anthracenylcarbonyl)[1,4′-bipiperidin]-3-yl]-4-morpholinyl-methanone hydrochloride
CAS Number: 591778-70-0
Empirical Formula (Hill Notation): C30H35N3O3 · HCl
Molecular Weight: 522.08
MDL Number: MFCD28167776
Linear Formula: C30H35N3O3 · HCl
Product Type: Chemical
| assay |
≥95% (HPLC) |
| color |
white to beige |
| form |
powder |
| InChI |
1S/C30H35N3O3.ClH/c34-29(32-16-18-36-19-17-32)24-8-5-13-33(21-24)25-11-14-31(15-12-25)30(35)28-26-9-3-1-6-22(26)20-23-7-2-4-10-27(23)28;/h1-4,6-7,9-10,20,24-25H,5,8,11-19,21H2;1H/t24-;/m1./s1 |
| InChI key |
DUBNXJIOBFRASV-GJFSDDNBSA-N |
| Quality Level |
100  |
| SMILES string |
O=C(C1=C2C=CC=CC2=CC3=CC=CC=C31)N(CC4)CCC4N5C[C@H](C(N6CCOCC6)=O)CCC5.[H]Cl |
| solubility |
H2O: 2 mg/mL, clear (warmed) |
| storage condition |
desiccated |
| storage temp. |
room temp |
| Application: |
CP-640186 hydrochloride has been used as an allosteric acetyl-CoA carboxylase (ACC) inhibitor (ACCi) for pharmacological inhibition of lipogenesis to determine if fatty acid synthesis is essential for brown adipose tissue (BAT) whitening. It has also been used as an inhibitor of mammalian acetyl-CoA carboxylase (mACC1/2) to study its effect on meropenem potency against the persisters from multiple pathogens, including B. thailandensis, P. aeruginosa, S.Typhimurium, and attenuated Y. pestis. |
| Biochem/physiol Actions: |
CP-640186 is a potent and orally active acetyl-CoA carboxylase 1/2 (ACC-alpha/beta, ACC1/2) inhibitor (IC50 ~50 nM) that targets the carboxyltransferase (CT) domain at the ACC dimer interface (via tight interactions with the putative biotin-binding site) in a reversible manner, uncompetitive with respect to ATP, and non-competitive with respect to bicarbonate, acetyl-CoA, and citrate. CP-610431 inhibits fatty acid (FA) synthesis, triglyceride (TG) synthesis, TG and apoB secretion (IC50 = 1.6, 1.8, 3.0, and 5.7 μM, respectively), but not cholesterol synthesis or apoC3 secretion in HepG2 cells (ACC1), as well as stimulates FA oxidation in C2C12 cells (ACC2) and in rat epitrochlearis muscle strips (EC50 = 57 nM and 1.3 μM, respectively). Oral administration is shown to inhibit FA synthesis in rats, CD1 mice, and ob/ob mice (ED50 = 13, 11, and 4 mg/kg, respectively) and stimulate rat whole body FA oxidation (ED50 ∼30 mg/kg) in vivo. |
| RIDADR |
NONH for all modes of transport |
| WGK Germany |
WGK 3 |
| Purity |
≥95% (HPLC) |
| Storage Temp. |
room temp |
| UNSPSC |
41121800 |
