DZ2002CAS# 33231-14-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 33231-14-0 | SDF | Download SDF |
PubChem ID | 11658872 | Appearance | Powder |
Formula | C10H13N5O3 | M.Wt | 251.24 |
Type of Compound | N/A | Storage | Desiccate at -20°C |
Solubility | DMSO : ≥ 61 mg/mL (242.80 mM) *"≥" means soluble, but saturation unknown. | ||
Chemical Name | methyl 4-(6-aminopurin-9-yl)-2-hydroxybutanoate | ||
SMILES | COC(=O)C(CCN1C=NC2=C1N=CN=C2N)O | ||
Standard InChIKey | HNKGMGPCSSJYOT-UHFFFAOYSA-N | ||
Standard InChI | InChI=1S/C10H13N5O3/c1-18-10(17)6(16)2-3-15-5-14-7-8(11)12-4-13-9(7)15/h4-6,16H,2-3H2,1H3,(H2,11,12,13) | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
DZ2002 Dilution Calculator
DZ2002 Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 3.9803 mL | 19.9013 mL | 39.8026 mL | 79.6052 mL | 99.5064 mL |
5 mM | 0.7961 mL | 3.9803 mL | 7.9605 mL | 15.921 mL | 19.9013 mL |
10 mM | 0.398 mL | 1.9901 mL | 3.9803 mL | 7.9605 mL | 9.9506 mL |
50 mM | 0.0796 mL | 0.398 mL | 0.7961 mL | 1.5921 mL | 1.9901 mL |
100 mM | 0.0398 mL | 0.199 mL | 0.398 mL | 0.7961 mL | 0.9951 mL |
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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DZ2002 is a potent and reversible S-Adenosyl-L-homocysteine Hydrolase(SAHH; AdoHcy Hydrolase) inhibitor with Ki of 17.9 nM. IC50 value: 17.9 nM(Ki) [1] Target: AdoHcy Hydrolase inhibitor in vitro: The cytotoxicity of DZ2002 is significantly less than DHCaA with an IC50 of 100 to 600 μM compared with 6 to 14 μM and shows very little cytotoxicity up to 100 μM. DZ2002 had little effects on lymphocyte proliferation (0.1 μM = 150,604 ± 13,862, 1 μM = 159,894 ± 11,152, and 10 μM = 136,157 ± 21,943 cpm) versus untreated Con A-stimulated cells (168,725 ± 8025 cpm). Similarly, little effect was seen in regards to IL-2 production from DZ2002-treated cells (0.1 μM = 1,838 ± 88, 1 μM = 1,793 ± 58, and 10 μM = 1,731 ± 36 pg/ml) versus untreated Con A-stimulated cells (1,806 ± 43 pg/ml). Although DZ2002 had little effect when T cells were stimulated with Con A, DZ2002 suppressed the MLR by 24.5, 42.3, and 46.0% at dosages of 0.1, 1, and 10 μM, respectively [1]. DZ2002 (500 μmol/L) significantly suppressed TLR agonists-stimulated up-regulation in IL-6, IL-12p40, TNF-α, and IgG and IgM secretion as well as in HLA-DR and CD40 expression of dendritic cells among human PBMCs in vitro. DZ2002 (100 μmol/L) also significantly suppressed TLR agonists-stimulated up-regulation in IL-6 and IL-23p19 production in murine BMDCs, and prevented Th17 differentiation and suppressed IL-17 secretion by the T cells in a BMDC-T cell co-culture system [3]. in vivo: As compared with controls, consecutive 7-day i.p. injections of DZ2002 inhibited hemolysis by 24.5 and 18.4% at doses of 0.08 and 2 mg/kg, respectively, thus decreasing anti-SRBC antibody production in vivo [1]. Male C57BL/6 mice immunized with ovalbumin (OVA) were treated with DZ2002 (1, 5, and 25 mg/kg/day) after which lymphocyte proliferation, cytokine production, and IgG responses to OVA were monitored. Administration of DZ2002 dose dependently suppressed OVA-specific lymphocyte proliferation and anti-OVA IgG production compared with controls [2]. Treatment of the mice with DZ2002 significantly attenuated the progression of glomerulonephritis and improved the overall health. In ex vivo studies, treatment of the mice with DZ2002 suppressed the development of pathogenic Th17 cells, significantly decreased IL-17, TGF-β, IL-6, and IL-23p19 production and impeded activation of the STAT3 protein and JNK/NF-κB signaling in splenocytes [3].
References:
[1]. Wu QL, et al. Inhibition of S-adenosyl-L-homocysteine hydrolase induces immunosuppression. J Pharmacol Exp Ther. 2005 May;313(2):705-11.
[2]. Fu YF, et al. S-adenosyl-L-homocysteine hydrolase inactivation curtails ovalbumin-induced immune responses. J Pharmacol Exp Ther. 2006 Mar;316(3):1229-37.
[3]. He SJ, et al. Therapeutic effects of DZ2002, a reversible SAHH inhibitor, on lupus-prone NZB×NZW F1 mice via interference with TLR-mediated APC response. Acta Pharmacol Sin. 2014 Feb;35(2):219-29.
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Therapeutic effects of DZ2002, a reversible SAHH inhibitor, on lupus-prone NZBxNZW F1 mice via interference with TLR-mediated APC response.[Pubmed:24374810]
Acta Pharmacol Sin. 2014 Feb;35(2):219-29.
AIM: To examine the therapeutic effects and underlying mechanisms of DZ2002, a reversible S-adenosyl-L-homocysteine hydrolase (SAHH) inhibitor, on lupus-prone female NZBxNZW F1 (NZB/W F1) mice. METHODS: Female NZB/W F1 mice were treated orally with DZ2002 (0.5 mg.kg(-1).d(-1)) for 11 weeks, and the proteinuria level and body weight were monitored. After the mice ware euthanized, serum biochemical parameters and renal damage were determined. Splenocytes of NZB/W F1 mice were isolated for ex vivo study. Toll-like receptor (TLR)-stimulated human peripheral blood mononuclear cells (PBMCs) or murine bone marrow-derived dendritic cells (BMDCs) were used for in vitro study. RESULTS: Treatment of the mice with DZ2002 significantly attenuated the progression of glomerulonephritis and improved the overall health. The improvement was accompanied by decreased levels of nephritogenic anti-dsDNA IgG2a and IgG3 antibodies, serum IL-17, IL-23p19 and TGF-beta. In ex vivo studies, treatment of the mice with DZ2002 suppressed the development of pathogenic Th17 cells, significantly decreased IL-17, TGF-beta, IL-6, and IL-23p19 production and impeded activation of the STAT3 protein and JNK/NF-kappaB signaling in splenocytes. DZ2002 (500 mumol/L) significantly suppressed TLR agonists-stimulated up-regulation in IL-6, IL-12p40, TNF-alpha, and IgG and IgM secretion as well as in HLA-DR and CD40 expression of dendritic cells among human PBMCs in vitro. DZ2002 (100 mumol/L) also significantly suppressed TLR agonists-stimulated up-regulation in IL-6 and IL-23p19 production in murine BMDCs, and prevented Th17 differentiation and suppressed IL-17 secretion by the T cells in a BMDC-T cell co-culture system. CONCLUSION: DZ2002 effectively ameliorates lupus syndrome in NZB/W F1 mice by regulating TLR signaling-mediated antigen presenting cell (APC) responses.
Synthesis and biological evaluation of immunosuppressive agent DZ2002 and its stereoisomers.[Pubmed:18815049]
Bioorg Med Chem. 2008 Oct 15;16(20):9212-6.
DZ2002 and its related stereoisomers were efficiently synthesized. The optical data of (R)- and (S)-DZ2002 were disclosed here for the first time. Their inhibitory potency was evaluated on SAHase and MLR assay in the mean time. In accordance with respective inhibitory potency of SAHase, the immunosuppressive potency order was demonstrated as (S)-DZ2002>(Rac)-DZ2002>(R)-DZ2002>(Keto)-DZ2002. These results indicate (S)-configuration of 2-chiral center in DZ2002 is important for binding with SAHase.