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  • Brand : BIOFRON

  • Catalogue Number : BN-O1179

  • Specification : 98%(HPLC)

  • CAS number : 1125-60-6

  • Formula : C9H8N2

  • Molecular Weight : 144.17

  • PUBCHEM ID : 70766

  • Volume : 5mg

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Catalogue Number


Analysis Method





Molecular Weight



Botanical Source

Structure Type





5-Isoquinolinamine/Isochinolin-5-amin/isoquinolin-5-amine/5-Amino Isoquinoline/Isoquinoline, 5-amino-/5-Aminoisoquinoline




1.2±0.1 g/cm3


Flash Point

183.3±8.1 °C

Boiling Point

335.7±17.0 °C at 760 mmHg

Melting Point

127-130 °C


InChl Key


WGK Germany


HS Code Reference

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:1125-60-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




The SH2-containing inositol-5′-phosphatase 1 (SHIP1) metabolizes PI(3,4,5)P3 to PI(3,4)P2. SHIP1-deficient mice exhibit progressive inflammation. Pharmacological activation of SHIP1 is emerging as a potential therapy for pulmonary inflammatory diseases. Here we characterize the efficacy of AQX-1125, a small-molecule SHIP1 activator currently in clinical development.

Experimental Approach
The effects of AQX-1125 were tested in several in vitro assays: on enzyme catalytic activity utilizing recombinant human SHIP1, on Akt phosphorylation in SHIP1-proficient and SHIP1-deficient cell lines, on cytokine release in murine splenocytes, on human leukocyte chemotaxis using modified Boyden chambers and on β-hexosaminidase release from murine mast cells. In addition, pharmacokinetic and drug distribution studies were performed in rats and dogs.

AQX-1125 increased the catalytic activity of human recombinant SHIP1, an effect, which was absent after deletion of the C2 region. AQX-1125 inhibited Akt phosphorylation in SHIP1-proficient but not in SHIP1-deficient cells, reduced cytokine production in splenocytes, inhibited the activation of mast cells and inhibited human leukocyte chemotaxis. In vivo, AQX-1125 exhibited >80% oral bioavailability and >5 h terminal half-life.

Consistent with the role of SHIP1 in cell activation and chemotaxis, the SHIP1 activator AQX-1125 inhibits Akt phosphorylation, inflammatory mediator production and leukocyte chemotaxis in vitro. The in vitro effects and the pharmacokinetic properties of the compound make it a suitable candidate for in vivo testing in various models of inflammation.

Linked Article
This article is accompanied by Stenton et al., pp. 1519-1529 of this issue. To view this article visit http://dx.doi.org/10.1111/bph.12038


SHIP1, inflammation, pulmonary, chemotaxis, PI3K, cell motility, phosphatidylinositol


Characterization of AQX-1125, a small-molecule SHIP1 activator Part 1. Effects on inflammatory cell activation and chemotaxis in vitro and pharmacokinetic characterization in vivo


Grant R Stenton, Lloyd F Mackenzie, Patrick Tam, Jennifer L Cross, Curtis Harwig, Jeffrey Raymond, Judy Toews, Joyce Wu, Nancy Ogden, Thomas MacRury, and Csaba Szabo

Publish date

2013 Mar;




The efficacy of AQX-1125, a small-molecule SH2-containing inositol-5′-phosphatase 1 (SHIP1) activator and clinical development candidate, is investigated in rodent models of inflammation.

Experimental Approach
AQX-1125 was administered orally in a mouse model of passive cutaneous anaphylaxis (PCA) and a number of rodent models of respiratory inflammation including: cigarette smoke, LPS and ovalbumin (OVA)-mediated airway inflammation. SHIP1 dependency of the AQX-1125 mechanism of action was investigated by comparing the efficacy in wild-type and SHIP1-deficient mice subjected to an intrapulmonary LPS challenge.

AQX-1125 exerted anti-inflammatory effects in all of the models studied. AQX-1125 decreased the PCA response at all doses tested. Using bronchoalveolar lavage (BAL) cell counts as an end point, oral or aerosolized AQX-1125 dose dependently decreased the LPS-mediated pulmonary neutrophilic infiltration at 3-30 mg kg−1 and 0.15-15 μg kg−1 respectively. AQX-1125 suppressed the OVA-mediated airway inflammation at 0.1-10 mg kg−1. In the smoke-induced airway inflammation model, AQX-1125 was tested at 30 mg kg−1 and significantly reduced the neutrophil infiltration of the BAL fluid. AQX-1125 (10 mg kg−1) decreased LPS-induced pulmonary neutrophilia in wild-type mice but not in SHIP1-deficient mice.

The SHIP1 activator, AQX-1125, suppresses leukocyte accumulation and inflammatory mediator release in rodent models of pulmonary inflammation and allergy. As shown in the mouse model of LPS-induced lung inflammation, the efficacy of the compound is dependent on the presence of SHIP1. Pharmacological SHIP1 activation may have clinical potential for the treatment of pulmonary inflammatory diseases.

Linked Article
This article is accompanied by Stenton et al., pp. 1506-1518 of this issue. To view this article visit http://dx.doi.org/10.1111/bph.12039


SHIP1, inflammation, pulmonary, chemotaxis, PI3K, COPD, asthma


Characterization of AQX-1125, a small-molecule SHIP1 activator Part 2. Efficacy studies in allergic and pulmonary inflammation models in vivo


Grant R Stenton, Lloyd F Mackenzie, Patrick Tam, Jennifer L Cross, Curtis Harwig, Jeffrey Raymond, Judy Toews, David Chernoff, Thomas MacRury, and Csaba Szabo

Publish date

2013 Mar;




Cholangiocarcinoma (CCA) is a rare, aggressive and highly lethal tumor. The disease is very difficult to diagnose and multi-modality treatments are ineffective. To improve our understanding of the biological characteristics of CCA, and facilitate the identification of valid treatments, an in-depth characterization of two novel Chinese patient-derived primary CCA cell lines was performed.

Two CCA cell lines were developed and labelled ZJU-0826 and -1125. The two cell lines were characterized with respect to phenotypic, molecular, biomarker, functional and histological properties.

Two novel cell lines were cultured for 2 years, and maintained for more than 100 passages. They retained their typical biliary epithelial morphology and ultrastructure. The population doubling times of ZJU-0826, and -1125 were 63.84 h and 44.73 h, respectively. The cells exhibited near-triploid karyotypes with complex structural aberrations. ZJU-1125 cells had mutations in TP53 exons. Short tandem repeats genotyping confirmed the human origin and difference between lines. An immunophenotype analysis showed that ZJU-0826 is positive for CD44, CD29, Pdx1, CD236, FoxA1, FoxA2, and Nanog, and ZJU-1125 positive for CD44, CD29, CD133, Pdx1, FoxA1, FoxA2, and Nanog. ZJU-1125 had greater invasion ability in vitro and tumorigenicity than those of ZJU-0826.

Our results confirm the validity of the ZJU-0826 and -1125 as representative models for the elucidation of the molecular pathogenesis of perihilar CCA, and intrahepatic CCA in both in vitro and in vivo studies, respectively.

Electronic supplementary material
The online version of this article (10.1245/s10434-019-07649-5) contains supplementary material, which is available to authorized users.


Establishment and Characterization of Two Novel Cholangiocarcinoma Cell Lines


Yanhua Zhang, MS,1 Jingfeng Luo, PhD,2 Xue Dong, MS,2 Fang Yang, MD,1 Miaofeng Zhang, MS,3 Juanjuan Zhao, PhD,4 Qiangfeng Wang, MD,5 Fei Zhou, MS,corresponding author2 Jihong Sun, MD,corresponding author2 and Xiaoming Yang, PhDcorresponding author2,6

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