Chitohexaose hexahydrochloride 

Chitohexaose hexahydrochloride is a small molecular polysaccharide. Chitohexaose hexahydrochloride inhibits the binding of AgW to TLR4. Chitohexaose hexahydrochloride upregulates IL-10, inhibits LPS-induced upregulation of ROS, induces alternative activation of macrophages/monocytes, and suppresses LPS-induced production of TNF-α, IL-1β and IL-6. Chitohexaose hexahydrochloride reverses the mortality of mice challenged with APAP or LPS. Chitohexaose hexahydrochloride can be used in research related to Acetaminophen (HY-66005)-induced hepatotoxicity and endotoxemia^[1][2].

Chitohexaose (48 h) does not activate the canonical inflammatory pathway in bone marrow-derived macrophages (BMDMs) from BALB/c mice, but potently inhibits LPS-induced production of proinflammatory mediators and reactive oxygen species (ROS). Meanwhile, it induces alternative activation of macrophages by upregulating Ym-1, Arginase-1, and interleukin-10 (IL-10)^[2].
Chitohexaose (10 μg/mL; 48 h) does not trigger inflammatory activation in PBMC-derived monocytes, but inhibits LPS-induced proinflammatory cytokine production and induces alternative activation by promoting IL-10 release and arginase activity^[2].

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

Chitohexaose (10 mg/kg; i.p.; single dose, double dose; administered concurrently with acetaminophen treatment, administered 6 h after acetaminophen treatment, administered at 6 and 18 h after acetaminophen treatment) protects male C57BL/6 mice against acetaminophen-induced acute liver injury. Among these regimens, the protocol of i.p. injection of two doses of 10 mg/kg at 6 and 18 h after acetaminophen challenge increases the survival rate of mice to 83%, while also alleviating liver necrosis, inflammasome activation and hepatic inflammation^[1].
Chitohexaose (10 mg/kg; i.p.; single dose; administered concurrently with APAP + LPS) reduces the mortality rate of acute liver failure induced by APAP + LPS in male C57BL/6 mice; when administered as a single i.p. dose of 10 mg/kg concurrently with the toxin combination, it achieves a 50% survival rate in mice, while also reducing liver enzyme levels and alleviating systemic inflammation^[1].
Chitohexaose (250 μg; i.p.) inhibits lipopolysaccharide (LPS)-induced production of proinflammatory mediators and increases the level of the anti-inflammatory cytokine IL-10 in BALB/c mice with endotoxemia^[2].

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

1203.72

C₃₆H₇₄Cl₆N₆O₂₅

127171-88-4

Solid

White to off-white

OC[C@@H](O[C@H]1O[C@@H]([C@@H]([C@H]2N)O)[C@H](O[C@H]2O[C@H]([C@H](O)CO)[C@H](O)[C@@H](N)C=O)CO)[C@H]([C@@H]([C@H]1N)O)O[C@@H]([C@@H]([C@H]3O)N)O[C@@H]([C@H]3O[C@@H]([C@@H]([C@H]4O)N)O[C@@H]([C@H]4O[C@@H]([C@@H]([C@H]5O)N)O[C@@H]([C@H]5O)CO)CO)CO.Cl.Cl.Cl.Cl.Cl.Cl

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Barman PK, et al. Chitohexaose protects against acetaminophen-induced hepatotoxicity in mice. Cell Death Dis. 2016;7(5):e2224. Published 2016 May 12.

  [2]. Panda SK, et al. Chitohexaose activates macrophages by alternate pathway through TLR4 and blocks endotoxemia. PLoS Pathog. 2012;8(5):e1002717.  [Content Brief]