Hecubine 

Hecubine is a monoterpene indole alkaloid found in Ervatamia ocinalis. Hecubine activates TREM2 expression, reduces LPS (HY-D1056)-stimulated inammatory cytokines (TNF-α、IL-6、IL-1β) overexpression, as well as suppresses the levels of TLR4-, MyD88-, MAPK/PI3K/AKT- and NF-κB-related proteins. Hecubin also exhibits antioxidative effect, reduces ROS production and activates of the Nrf2/HO-1 pathway. Hecubine rescues LPS-induced behavioral deficits in zebrash larvae. Hecubine can be used for the research of neural inflammation-associated central nervous system diseases^[1].

Hecubine directly binds to purified TREM2 protein with a binding affinity of -7.07 ± 0.03 kcal/mol^[1].
Hecubine (25 μM; 1 h) directly interacts with TREM2 in BV2 microglial cells, increasing the protein's thermal stability by shifting its T_m by 6.4 ± 0.7 °C^[1].
Hecubine (0.7-50 μM; 1 h pretreatment, followed by 24 h LPS stimulation) inhibits LPS (HY-D1056)-induced NO production in BV2 microglial cells with an IC₅₀ of ~6 μM, achieving 52.1%, 64.6%, and 73.8% inhibition at 6, 12, and 25 μM respectively^[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by 24 h LPS stimulation) suppresses LPS-induced production of pro-inflammatory mediators (PGE₂, TNF-α, IL-6, IL-1β) and restores IL-10 levels in BV2 microglial cells, with maximal effects at 25 μM including reducing PGE₂ to 15.3% and IL-6 to <8.8% of LPS-treated levels^[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by LPS stimulation) upregulates TREM2 expression, downregulates TLR4/MyD88 signaling, inhibits MAPK/PI3K/AKT and NF-κB pathway activation, and reduces iNOS/COX-2 expression in LPS-stimulated BV2 microglial cells, with 25 μM Hecubine suppressing p38/AKT phosphorylation and NF-κB p65 nuclear translocation by ~45%, ~45.6%, and ~40.1% respectively^[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by LPS stimulation) inhibits LPS-induced ROS production in BV2 microglial cells in a dose-dependent manner^[1].
Hecubine (6-25 μM; 1 h pretreatment, followed by LPS stimulation; or 1 h treatment alone) activates the Nrf2/HO-1 antioxidant pathway in BV2 microglial cells, with 25 μM Hecubine increasing Nrf2 and HO-1 expression by 4.45-fold and 8.69-fold respectively in LPS-stimulated cells, and increasing expression of both proteins in a dose-dependent manner in unstimulated cells^[1].

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

Hecubine (6-25 μM; continuous exposure; 24 hours prior to LPS injection) reverses LPS (HY-D1056)-induced neuroinflammation, oxidative stress, and behavioral deficits in zebrash larvae by activating TREM2 and Nrf2/HO-1 signaling and inhibiting pro-inflammatory mediator production^[1].

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

310.43

C₂₀H₂₆N₂O

62874-52-6

CC[C@@]12[C@@]3([H])[C@](C[N@](CCC4=C(N(C5=CC=CC=C54)C)CC2)C1)([H])O3

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Li L, Xu N, Wang X, et al. Hecubine suppresses lipopolysaccharide-stimulated neuroinflammation and oxidative stress by targeting TREM2 and regulating Nrf2/TLR4 signaling in vitro and in vivo[J]. 2023.