HX 531

Product NameHX 531
CAS188844-34-0
MFC29H29N3O4
MW483.56
EINECS
MOL File188844-34-0.mol

Chemical Properties

Boiling point	656.2±55.0 °C(Predicted)
Density	1.27±0.1 g/cm3(Predicted)
storage temp.	2-8°C
solubility	DMF:15.0(Max Conc. mg/mL);31.02(Max Conc. mM) DMF:PBS (pH 7.2) (1:6):0.14(Max Conc. mg/mL);0.29(Max Conc. mM) DMSO:17.67(Max Conc. mg/mL);36.53(Max Conc. mM) Ethanol:0.12(Max Conc. mg/mL);0.25(Max Conc. mM)
form	A crystalline solid
pka	3.70±0.10(Predicted)
color	Light yellow to orange

Usage And Synthesis

Uses

HX 531 is a novel RXR antagonist used to enhance transactivation of PPARγ and ST 13 preadipocyte differentiation. Helps in the reduction of triglyceride content in white adipose tissue, skeletal muscle and liver.

Biological Activity

HX-531 is a potent antagonist of the retinoid X receptor (RXR) with an IC50 value of 18 nM. HX531 has been used in many studies of the various effects of retinoids and RXR activity in diseases such as diabetes, Parkinsonμs disease, often as a control for agonists such as Bexarotene. It was recently shown to promote white adipogenic differentiation and inhibit both basal and Bexarotene-induced brown adipogenic differentiation.

in vivo

HX531 (0.1% and 0.3% food additive, oral, for two weeks) prevents weight gain in mice on a high-fat diet and stops high blood sugar and high insulin levels induced by the high-fat diet, while increasing leptin levels^[2].
HX531 (0.1% and 0.3% food additive, oral, for two weeks) blocks the enlargement of fat cells and alleviates insulin resistance^[2].
HX531 (0.1% and 0.3% food additive, oral, for two weeks) directly antagonizes PPARγ/RXR, reducing molecules involved in fatty acid influx and fat formation in skeletal muscle, while increasing molecules involved in energy expenditure^[2].
HX531 (0.1% and 0.3% food additive, oral, for 3-4 weeks) leads to a rebound in high blood sugar and insulin resistance associated with fat atrophy^[2].
HX531 (10mg/kg, oral, daily, for 30 weeks) reduces body weight in rats, inhibits fat cell enlargement, and induces G0/G1 cell cycle arrest in fat cells^[3].

Animal Model:	KKAy mouse induced by HF or HC^[2]
Dosage:	0.1% and 0.3% food additive, 2 weeks
Administration:	Oral
Result:	Reduced the body weight of mice, fasting blood glucose, fasting plasma insulin, and insulin tolerance. Increased Rectal temperature, rosed oxygen consumption , and serum leptin levels went up. Lowered the expression of fatty acid translocase/CD36, increased the expression of β3-adrenergic receptors (β3-AR), and decreased free fatty acids (FFA), TNF-α, and resistin. Reduced the expression of lipogenic enzymes SREBP1 and SCD1, increased the expression of molecules involved in fatty acid burning like ACO, and molecules that dissipate energy like UCP2, lowered long-chain FA-CoA and triglyceride levels in muscle.

Animal Model:	PPARγ deficient mice ^[2]
Dosage:	0.1% and 0.3% food additive, 3 and 4 weeks
Administration:	Oral
Result:	Prevented the reoccurrence of high blood sugar and insulin resistance associated with fatty atrophy.

Animal Model:	LETO and OLETF rats^[3]
Dosage:	10 mg/kg, daily, 30 weeks
Administration:	Oral
Result:	Suppressed weight gain and reduced the excretion of urinary albumin.Led to G0/G1 cell cycle arrest, inhibited adipocyte hypertrophy, and suppressed the proliferation activity of fat cells.

storage

Store at +4°C

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