| Size | Price | Stock | Qty |
|---|---|---|---|
| 5mg |
|
||
| 10mg |
|
||
| 25mg |
|
||
| 50mg |
|
||
| 100mg |
|
||
| 250mg |
|
||
| Other Sizes |
|
Purity: ≥98%
AMI-1 (AMI 1) disodium salt is a novel, cell-permeable and selective inhibitor of Histone Methyltransferase (HMT) with anti-inflammatory activity. It inhibits HMT with an IC50 of 3.0 μM and 8.8 μM for yeast Hmt1p and human PRMT1, respectively.
| ln Vitro |
The in vitro methylation reactions carried out by the five recombinantly active PRMTs (PRMT1, -3, -4, and -6 as well as Hmt1p) can be inhibited by AMI-1[2]. AMI-1 inhibits type II PRMT5 in addition to type I PRMTs (PRMT1, 3, 4, and 6)[2]. AMI-1 does not compete with AdoMet for the binding site and selectively inhibits the methyltransferase activity of arginine in vitro, but not that of lysine[3]. Cellular proteins and GFP-Npl3 methylation are both inhibited by AMI-1[3]. In vitro, sarcoma in S180 and U2OS cells is inhibited by AMI-1 (0.6-2.4 mM; 48-96 hours) in a time- and dose-dependent manner[4]. AMI-1 (1.2–2.4 mM; 48–72 hours) induces apoptosis in cells, which lowers the viability of S180 cells[4].
|
|---|---|
| ln Vivo |
AMI-1 reduces S180 viability in vivo at a dose of 0.5 mg intraperitoneally every day for seven days[4]. ?In a tumor xenograft model, AMI-1 (0.5 mg; intratumorally; daily; for 7 days) downregulates PRMT5 but does not control PRMT7 expression[4]. ?In a tumor xenograft model, AMI-1 (0.5 mg; intratumorally; daily; for 7 days) reduces the levels of H4R3me2s and H3R8me2s[4].
|
| Cell Assay |
Cell Viability Assay[4]
Cell Types: S180 cells, U2OS cells Tested Concentrations: 0.6 mM, 1.2 mM, 2.4 mM Incubation Duration: 48 hrs (hours), 72 hrs (hours), 96 hrs (hours) Experimental Results: Inhibited the cell viability. Increased the percentages of cells undergoing apoptosis. |
| Animal Protocol |
Animal/Disease Models: 6-7 weeks old male Kunming mice (18-22 g), with S180 cells xenograft[4]
Doses: 0.5 mg Route of Administration: Intratumorally, daily, for 7 days Experimental Results: diminished tumor weight. |
| References |
[1]. Zhang, B., et al. Targeting protein arginine methyltransferase 5 inhibits colorectal cancer growth by decreasing arginine methylation of eIF4E and FGFR3. Oncotarget. 2015 Sep 8;6(26):22799-811.
[2]. Baolai Zhang, et al. Arginine Methyltransferase inhibitor-1 Inhibits Sarcoma Viability in vitro and in vivo. Oncol Lett. 2018 Aug;16(2):2161-2166. [3]. Donghang Cheng, et al. Small Molecule Regulators of Protein Arginine Methyltransferases. J Biol Chem. 2004 Jun 4;279(23):23892-9. |
| Molecular Formula |
C21H14N2NA2O9S2
|
|
|---|---|---|
| Molecular Weight |
548.45
|
|
| CAS # |
20324-87-2
|
|
| Related CAS # |
AMI-1 free acid;134-47-4
|
|
| SMILES |
O=C(NC1=CC2=CC(S(=O)([O-])=O)=CC(O)=C2C=C1)NC3=CC4=CC(S(=O)([O-])=O)=CC(O)=C4C=C3.[Na+].[Na+]
|
|
| Chemical Name |
|
|
| Synonyms |
|
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
|
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
|
|||
|---|---|---|---|---|
| Solubility (In Vivo) |
|
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 1.8233 mL | 9.1166 mL | 18.2332 mL | |
| 5 mM | 0.3647 mL | 1.8233 mL | 3.6466 mL | |
| 10 mM | 0.1823 mL | 0.9117 mL | 1.8233 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
TGF-β is the main component in ISEM that induced PRMT1 upregulation in fibroblasts. ISEM from epithelial cells, TGF-β Ab, and TGF-β Ab were used to stimulate HFL1 cells, and the expressions ofprmt1,cox2, andvegfwere detected by RT-qPCR (A–C). The expressions of PRMT1 and COX2 protein were detected by Western blot (DandE). TGF-β with or without AMI-1 (5 and 10 μM), the pan PRMT enzymatic activity inhibitor, was used to stimulate HFL1, and COX2 expression was detected by Western blot (F).J Immunol.2015 Jul 1;195(1):298-306. |
Expressions ofcox2andvegfand concentrations of IgE and NO in serum from chronic AIPI rats with or without AMI-1 administration. The expressions ofcox2(A) andvegf(B) were detected by RT-qPCR in lung tissues from control rats, AIPI rats, and AIPI rats with administration of AMI-1. Total IgE (C) and NO concentrations (D) in serum were detected by ELISA and the Griess method.J Immunol.2015 Jul 1;195(1):298-306. |
Histopathological changes and remodeling in chronic AIPI rats with and without the administration of AMI-1. Representative images of the histopathological changes by H&E staining (A), PAS staining (B), and Masson staining (D) were from lung sections of E3 rats without Ag challenge, with Ag challenge for 8 wk, and with both Ag challenge and AMI-1 administration for 8 wk, respectively.J Immunol.2015 Jul 1;195(1):298-306. |
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
COA
