1. GPCR/G Protein
  2. Adenosine Receptor
  3. Norisoboldine

Norisoboldine (Synonyms: (+)-Laurelliptine)

Cat. No.: HY-N0586
Handling Instructions

Norisoboldine is an isoquinoline alkaloid which acts as an AhR agonist, and enhances the function of the adenosine A1 receptor.

For research use only. We do not sell to patients.

Norisoboldine Chemical Structure

Norisoboldine Chemical Structure

CAS No. : 23599-69-1

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Norisoboldine is an isoquinoline alkaloid which acts as an AhR agonist, and enhances the function of the adenosine A1 receptor.

In Vitro

Norisoboldine, dose-dependently, inhibits PMA and ionomycin-induced NFAT reporter gene expression in K562-luc cells in the range of 2-50 μM. Norisoboldine also inhibits PMA and ionomycin-induced NFAT dephosphorylation in K562-luc cells and Jurkat cells. Consequently, Norisoboldine suppresses PMA plus ionomycin-induced IL-2 expression in Jurkat cells[1]. Norisoboldine-treated Naive CD4+CD62L+ T cells show a markedly higher frequency of Treg cells, and lead to significant up-regulation of Foxp3 expression. The expression of IL-10 is up-regulated in Norisoboldine (30 μM)-treated naive T cells as compared to the control group. Norisoboldine (30 μM) markedly decreases the levels of IL-17A and IL-17F but not IL-21 in the supernatants of naive T cells. Norisoboldine induces the differentiation of Treg cells, and the expression of CYP1A1 in lymphocytes dependent on AhR. Norisoboldine promotes AhR/Hsp90 complex disassociation and AhR nuclear translocation in lymphocytes[2]. Norisoboldine (10, 30 μM) treatment does not affect the viability of CD4+ T cells, but markedly increase the number of Foxp3+ Treg cells. Notably, when TGF-β is absent, Norisoboldine also induces the differentiation of Treg cells. Norisoboldine increases the protein and mRNA level of TGF-β only at the higher dose of 40 mg, and it slightly affectes the level of IL-6[3]. Norisoboldine can stably bind to AhR, up-regulate the nuclear translocation of AhR, and enhance the accumulation of the AhR-ARNT complex, AhR-mediated reporter gene activity and CYP1A1 expression in RAW 264.7 cells. Norisoboldine inhibits the nuclear translocation of NF-κB-p65, resulting in the evident accumulation of the AhR-NF-κB-p65 complex, which can be markedly inhibited through either Res or α-NF[4]. Norisoboldine inhibits forskolin-induced cAMP accumulation in cultured spinal cord neurons through the adenosine A1 receptor[5].

In Vivo

Norisoboldine (10 mg/kg, i.p.), alleviates DNCB-induced dermatitis in mice, by the reduction of ear swelling and attenuation of inflammatory infiltration into ear tissue. Moreover, mRNA levels of INF-γ, TNF-α, IL-4 and IL-6 in ears of Norisoboldine-treated mice are reduced by 78.4, 77.8, 72.3 and 73.9%, respectively, compared with untreated controls[1]. The joints from the recipient mice that receive Norisoboldine-Treg exhibit a lower degree of inflammation and attenuated cartilage damage than those received Model-Treg. Moreover, Norisoboldine-Treg more obviously reduces the serum levels of IL-17 and elevates the levels of IL-10 in recipient mice. Mice that receive Norisoboldine-Treg show fewer Th17 cells and more Treg cells distribution in MLNs. Norisoboldine (40 mg/kg) yields a marked decrease in arthritis index and paw swelling. Norisoboldine (40 mg/kg) reduces the inflammation score and bone erosion score to 6.12±0.42 and 0.88±0.13, respectively. Norisoboldine (40 mg/kg) markedly lowers the levels of IgG and IgG2a, which can be largely counteracted by RES[2]. Norisoboldine (20, 40 mg/kg) markedly reduces the symptoms of colitis, the levels of IL-1β and TNF-α, and the activation of ERK, p38 MAPK and NF-κB-p65. Norisoboldine (20, 40 mg/kg) and 5-ASA (500 mg/kg) treatments markedly reduces MPO activity in colons of colitis mice[3]. Norisoboldine (80 mg/kg) decreases formalin-induced activation of extracellular signal-regulated kinase (ERK) and calmodulin-dependent protein kinase II (CaMKIIα) in the spinal cord via adenosine A1 receptor[5].

Molecular Weight







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Room temperature in continental US; may vary elsewhere.


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

Solvent & Solubility
In Vitro: 

DMSO : ≥ 62.5 mg/mL (199.46 mM)

*"≥" means soluble, but saturation unknown.

Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 3.1913 mL 15.9566 mL 31.9132 mL
5 mM 0.6383 mL 3.1913 mL 6.3826 mL
10 mM 0.3191 mL 1.5957 mL 3.1913 mL
*Please refer to the solubility information to select the appropriate solvent.
Cell Assay

CD4+ T cells are seeded at the density of 2×105 cells/mL into 96-well plates and treated with Norisoboldine (0.1, 1, 3, 10, 30, 60, 100 μM) for 68 h. Then, 20 μL of MTT solution (5 mg/mL) is added, and further incubated for 4 h. Subsequently, the supernatants are removed and the formazone crystals are dissolved using 150 μL of DMSO. The optical absorbance at 570 nm is read with a Model 1500 Multiskan Spectrum Microplate Reader.

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

Animal Administration

Briefly, mice are placed on a 50°C hotplate, and the time between placement and shaking or licking of the paws or jumping is recorded as a response latency. The cut-off time is 60 s to avoid tissue damage. Animals are screened before experiments, and the animals whose latency is between 10 and 30 s are then randomly divided into five groups: vehicle group, Norisoboldine (20 mg/kg) group, Norisoboldine (40 mg/kg) group, Norisoboldine (80 mg/kg) group and morphine (4 mg/kg) group. After administration of drugs, the latency of each mouse is tested again.

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

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