Product Name Citreorosein
CAS No.: 481-73-2
Catalog No.: CFN98750
Molecular Formula: C15H10O6
Molecular Weight: 286.2 g/mol
Purity: >=98%
Type of Compound: Anthraquinones
Physical Desc.: Yellow powder
Targets: cAMP | NF-kB | PI3K | Akt | COX | JNK | Phospholipase (e.g. PLA) | IkB | ERK | p38MAPK | AP-1 | p65 | IKK
Source: The roots and rhizomes of Rheum palmatum L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Citreorosein is a cAMP phosphodiesterase inhibitor, it has anti-inflammatory effect, inhibits proinflammatory cytokines production through the inhibition of both MAPKs and AKT-mediated IκB kinase (IKK) phosphorylation and subsequent inhibition of transcription factor NF-κB activation. Citreorosein attenuates degranulation and LTC(4) generation through the suppression of multiple step signaling and would be beneficial for the prevention of allergic inflammation.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to:

The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Mol Cell Biochem. 2012 Jun;365(1-2):333-41.
    Citreorosein inhibits degranulation and leukotriene C₄ generation through suppression of Syk pathway in mast cells.[Pubmed: 22395859]
    The aim of this study was to evaluate whether Citreorosein (CIT), a naturally occurring anthraquinone isolated from Polygoni cuspidati (P. cuspidati) radix, modulates degranulation and 5-lipoxygenase (5-LO)-dependent leukotriene C(4) (LTC(4)) generation in mast cells.
    Citreorosein suppresses both degranulation and the generation of LTC(4) in a dose-dependent manner in stem cell factor (SCF)-mediated mouse bone marrow-derived mast cells (BMMCs). With regard to its molecular mechanism of action, we investigated the effects of Citreorosein on intracellular signaling and mast cell activation employing BMMCs. Binding of SCF to c-Kit on mast cell membranes induced increases in intrinsic tyrosine kinase Syk activity and activation of multiple downstream events including phosphorylation of phospholipase Cγ (PLCγ), mobilization of intracellular Ca(2+), phosphatidylinositol 3-kinase (PI3K), Akt, MAP kinases (MAPKs), translocation of phospho-phospholipase A(2) (PLA(2)) and 5-LO.
    The results from the biochemical analysis demonstrate that Citreorosein attenuates degranulation and LTC(4) generation through the suppression of multiple step signaling and would be beneficial for the prevention of allergic inflammation.
    Biol Pharm Bull. 2012;35(6):938-45.
    Citreorosein inhibits production of proinflammatory cytokines by blocking mitogen activated protein kinases, nuclear factor-κB and activator protein-1 activation in mouse bone marrow-derived mast cells.[Pubmed: 22687535]
    Citreorosein (CIT), an anthraquinone component of Polygoni cuspidati (P. cuspidati) radix, suppressed gene expression of proinflammatory cytokines including tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β in mouse bone marrow-derived mast cells (BMMCs) stimulated with phorbol 12-myristate 13-acetate (PMA) plus the calcium ionophore A23187.
    To investigate the molecular mechanisms underlying Citreorosein inhibition of the pro-inflammatory cytokine production, its effects on the activation of both nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs) were assessed. Citreorosein attenuated phosphorylation of the MAPKs including extracellular signal-regulated kinase 1/2 (ERK1/2), p38 MAP kinase and c-Jun NH(2)-terminal kinase (JNK). Furthermore, Citreorosein strongly inhibited DNA binding activity of NF-κB through the inhibition of phosphorylation and degradation of inhibitor of kappaB (IκB) as well as activator protein-1 (AP)-1 through the reduction of phosphorylation of c-Jun.
    These results demonstrate that Citreorosein inhibits proinflammatory cytokines production through the inhibition of both MAPKs and AKT-mediated IκB kinase (IKK) phosphorylation and subsequent inhibition of transcription factor NF-κB activation, thereby attenuating the production of proinflammatory cytokines.
    Food Chem Toxicol. 2012 Mar;50(3-4):913-9.
    Citreorosein, a naturally occurring anthraquinone derivative isolated from Polygoni cuspidati radix, attenuates cyclooxygenase-2-dependent prostaglandin D2 generation by blocking Akt and JNK pathways in mouse bone marrow-derived mast cells.[Pubmed: 22154852]

    In this study, we examined the effects of Citreorosein (CIT), an anthraquinone component of Polygoni cuspidati radix (P. cuspidati, Polygonaceae), on cyclooxygenase (COX)-2 dependent prostaglandin (PG)D2 generation in mast cells, central effector cells of allergy and other inflammatory diseases. Citreorosein strongly inhibited COX-2-dependent PGD2 generation in a concentration-dependent manner in mouse bone marrow-derived mast cells (BMMCs) stimulated with stem cell factor (SCF)/IL-10/LPS. In an effort to identify the mechanisms underlying the inhibition of COX-2-dependent PGD2 generation by Citreorosein, we examined the effects of this compound on MAP kinases, Akt and NF-κB signaling pathways, which are essential for COX-2 induction. Citreorosein inhibited nuclear translocation of the nuclear factor (NF)-κB p65 subunit and its cognate DNA-binding activity, which correlated with its inhibitory effects on the phosphorylation of Akt and IKK and subsequent phosphorylation and degradation of IκB. Furthermore, Citreorosein significantly attenuated the DNA binding of activator protein (AP)-1 that regulates COX-2 expression through the reduction of the phosphorylation of c-Jun. Moreover, inhibition of PGD2 generation by Citreorosein was accompanied by a decrease in phosphorylation of cytosolic phospholipase A2α.
    Taken together, the present study suggests that Citreorosein represents a potential therapeutic approach for the treatment of inflammatory diseases.
    Arch Pharm Res. 2012 Mar;35(3):447-54.
    A facile synthesis of emodin derivatives, emodin carbaldehyde, citreorosein, and their 10-deoxygenated derivatives and their inhibitory activities on μ-calpain.[Pubmed: 22477191]

    A new procedure for the preparation of emodin carbaldehyde and Citreorosein was described, in which, ω,ω'-dibromomethylemodin triacetate was prepared as a key intermediate by NBSmediated bromination of 1,3,8-triacetylemodin. Reduction of emodin and Citreorosein with SnCl(2) in a 1:1 mixture of HOAc and HCl afforded the corresponding anthrones in 90% and 92% yield, respectively, while the corresponding 10-desoxyemodin carbaldehyde was prepared by MnO(2) oxidation of 10-desoxyCitreorosein.
    10-DesoxyCitreorosein and emodin carbaldehyde showed feasible μ-calpain inhibitory activities with IC(50) values of 20.15 and 25.77 M, respectively.
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