Aeroplysinin 1  (Synonyms: (+)-Aeroplysinin-1)

Aeroplysinin 1 ((+)-Aeroplysinin-1), a secondary metabolite isolated from marine sponges, shows potent antibiotic effects on Gram-positive bacteria and exerts antiviral activity against HIV-1 (IC₅₀=14.6 μM). Aeroplysinin 1 has anti-inflammatory, anti-angiogenic and anti-tumor activities. Aeroplysinin 1 induces apoptosis in endothelial cells^[1][2].

Aeroplysinin 1 shows anti-proliferative effect against tumor cells (HT-1080, HTC-116, HeLa, THP-1, NOMO-1 and HL-60 cells), with IC₅₀s ranging from 2.3 to 17 μM^[1].
Aeroplysinin-1 also exhibits an antiviral activity toward HIV-1 caused by inhibition of its reverse transcriptase activity^[1].
Aeroplysinin 1 inhibits P. phosphoreum, C. wailesii, P. minimum and HIV with IC₅₀s of 3.5, 5.6, 7.0 and 14.6 μM^[1].
Aeroplysinin 1 inhibits human endothelial cells (EVLC-2, HMEC, RF-24, and HUVEC cells), with IC₅₀s ranging from 2.6 to 4.7 μM^[2].
(+)-Aeroplysinin-1 (0.25-0.5 μM) blocks the EGF-dependent proliferation of both MCF-7 and ZR-75-1 human breast cancer cells and inhibits the ligand-induced endocytosis of the EGF receptor in vitro^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

338.98

C₉H₉Br₂NO₃

28656-91-9

Oil

Colorless to light yellow

N#CC[C@]1(O)C=C(Br)C(OC)=C(Br)[C@@H]1O

Room temperature in continental US; may vary elsewhere.

• [1]. García-Vilas JA, et al. Aeroplysinin-1, a Sponge-Derived Multi-Targeted Bioactive Marine Drug. Mar Drugs. 2015;14(1):1. Published 2015 Dec 22.  [Content Brief]

  [2]. Martínez-Poveda B, et al. The brominated compound aeroplysinin-1 inhibits proliferation and the expression of key pro- inflammatory molecules in human endothelial and monocyte cells. PLoS One. 2013;8(1):e55203.  [Content Brief]

  [3]. Kreuter MH, et al. Inhibition of intrinsic protein tyrosine kinase activity of EGF-receptor kinase complex from human breast cancer cells by the marine sponge metabolite (+)-aeroplysinin-1. Comp Biochem Physiol B. 1990;97(1):151‐158.  [Content Brief]