2. Apoptosis Immunology/Inflammation Metabolic Enzyme/Protease
  3. TNF Receptor Interleukin Related Arginase PD-1/PD-L1
  4. Naamidine J

Naamidine J is an imidazole-type alkaloids discovered in a sponge. Naamidine J inhibits inflammation by binding to the protein CSE1L (KD = 5.41 μM). Namidine J significantly inhibits the expression of pro-inflammatory factors such as TNF-α, IL-1β, and IL-6, and upregulates anti-inflammatory factors such as CD206 and Arg-1. Namidine J inhibits PD-L1 and shows antitumor activity. Namidine J significantly reduces pulmonary tissue edema, inflammatory cell infiltration and cytokine storm in mice. Namidine J can be used for the research on the immune microenvironment of acute lung injury and tumors.

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Naamidine J

Naamidine J Chemical Structure

CAS No. : 2227550-73-2

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Naamidine J Related Antibodies

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Description

Naamidine J is an imidazole-type alkaloids discovered in a sponge. Naamidine J inhibits inflammation by binding to the protein CSE1L (KD = 5.41 μM). Namidine J significantly inhibits the expression of pro-inflammatory factors such as TNF-α, IL-1β, and IL-6, and upregulates anti-inflammatory factors such as CD206 and Arg-1. Namidine J inhibits PD-L1 and shows antitumor activity. Namidine J significantly reduces pulmonary tissue edema, inflammatory cell infiltration and cytokine storm in mice. Namidine J can be used for the research on the immune microenvironment of acute lung injury and tumors[1][2].

IC50 & Target[2]

IL-1β

 

IL-6

 

In Vitro

Naamidine J (5 μM, 24 h) has cytotoxicity against K562 cells with an IC50 of 11.3 μM but is not toxic to macrophages and RKO cells (IC50 > 40 μM)[1][2].
Naamidine J (10 μM, 24 h) reduces PD-L1 expression in RKO cells and PDAC cells[1][3].
Naamidine J (1-5 μM, 5 h) inhibits the Inflammatory response in LPS (HY-D1056)-induced RAW264.7 macrophages[2].
Naamidine J (5 μM, 5 h) inhibits nuclear translocation of transcription factor SP1 mediated by CSE1L in LPS-induced macrophages[2].
Naamidine J (10 μM, 24 h) restores the cytotoxicity of CD8+ T cells and significantly reduce the survival of PDAC cells (MIA-PaCa2, BxPC-3)[3].

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

Naamidine J Related Antibodies

Western Blot Analysis[1]

Cell Line: RKO cells
Concentration: 10 μM
Incubation Time: 24 h
Result: Had a certain inhibitory effect on PD-L1 expression.

ELISA Assay[1]

Cell Line: RAW264.7 cells
Concentration: 1, 2 and 5 μM
Incubation Time: Pre-treatment for 3 hours, followed by co-stimulation with LPS for 2 hours
Result: Exhibited concentration-dependent inhibition of TNF-α release.

RT-PCR[1]

Cell Line: RAW264.7 cells
Concentration: 1, 2 and 5 μM
Incubation Time: Pre-treatment for 3 hours, followed by co-stimulation with LPS for 2 hours
Result: Inhibited pro-inflammatory factors (TNF-α, IL-1β, IL-6), and promoted anti-inflammatory factors (CD206, Arg-1).

Western Blot Analysis[1]

Cell Line: RAW264.7 cells
Concentration: 5 μM
Incubation Time: Pre-treatment for 3 hours, followed by co-stimulation with LPS for 2 hours
Result: Resulted in the accumulation of SP1 in the cytoplasm.
Enhanced the interaction between CSE1L and SP1.
In Vivo

Naamidine J (10-20 mg/kg, i.p., once daily for 3 days) significantly alleviates acute lung injury induced by LPS in mice, and reduced pulmonary edema [2].
Naamidine J (30 mg/kg, i.p., once every three days for 28 days) significantly enhances the proportion of CD8+ Tex subset and reduced the proportion of intermediate CD8+ Tex subset in mice bearing subcutaneous tumors with high NAT10 expression[3].

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

Animal Model: Acute lung injury model established in mice[2]
Dosage: 10 and 20 mg/kg
Administration: Intraperitoneal injection (i.p.), once daily for 3 days
Result: Significantly reduced the increase in lung organ coefficient induced by LPS and alleviate pulmonary edema.
Significantly improved the pathological damage of lung tissue and reduce the infiltration of inflammatory cells.
Significantly reduced the protein levels of TNF-α in serum and lung tissue, as well as the mRNA expression of various inflammatory factors.
Reduced the proportion of pro-inflammatory M1-type macrophages in the lung tissue and increased the proportion of anti-inflammatory M2-type macrophages.
Animal Model: PanO2 xenograft model established in four-week-old female C57BL/6 mice (18 to 20 g)[3]
Dosage: 30 mg/kg
Administration: Intraperitoneal injection (i.p.), once every three days for 28 days
Result: Significantly inhibited tumor growth in the Nat10-OE group.
Reversed T cell exhaustion and restores anti-tumor function.
Increased the infiltration of CD8+ T cells, reduced the PD-1 with IFNγ and exhausted phenotype, and increased the PD-1-IFNγ+ cytotoxic phenotype.
Molecular Weight

477.51

Formula

C25H27N5O5
CAS No.
SMILES

O=C1N=C(C(N1C)=O)NC2=NC(CC3=CC=C(C=C3)OC)=C(CC4=CC=C(C(OC)=C4)OC)N2C
Structure Classification
Initial Source

Pericharax heteroraphis
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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Naamidine J Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Naamidine J2227550-73-2TNF ReceptorInterleukin RelatedArginasePD-1/PD-L1Tumor Necrosis Factor ReceptorTNFRILPD-1/Programmed death-ligand 1Imidazole-type alkaloidsacute Lung Injurymice modelMacrophage-mediated InflammationInhibitorinhibitorinhibit

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