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| Targets |
The primary molecular target of 3-Deazaadenosine is S-adenosylhomocysteine hydrolase (SAHH), a key enzyme in the methionine cycle that hydrolyzes SAH to adenosine and homocysteine. The compound inhibits SAHH with a Ki value of 3.9 μM. By blocking SAHH activity, 3-Deazaadenosine causes the accumulation of SAH, a potent feedback inhibitor of S-adenosylmethionine (SAM)-dependent methyltransferases. This indirect inhibition of methyltransferases affects a wide range of cellular functions, including gene expression, signal transduction, and viral replication. It also modulates NF-κB signaling and inhibits key kinases within the Ras–ERK and PI3K–Akt pathways.
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| ln Vitro |
3-Deazaadenosine has a Ki of 3.9 µM, making it an inhibitor of S-adenosylhomocysteine hydrolase. 3-Deazaadenosine, with an IC50 of 0.15 and 0.20 µM, respectively, shows anti-HIV action and suppresses the p24 antigen in peripheral blood mononuclear (PBMC) cells infected with HIV-1 isolates (A012 and A018) [1]. 3-Deazaadenosine (1-100 µM) causes IκBα (but not IκBβ) to be broken down by proteases, increases the DNA-binding activity of NF-κB, and suppresses the production of TNF-α mRNA in RAW 264.7 cells. 3-Homocysteine increases the inhibitory impact of 3-deazaadenosine (100 µM), which increases NF-κB nuclear translocation but inhibits LPS-induced NF-κB transcriptional activity [2]. 3-Phosphorylation of Raf and ERK, protein-dependent kinase 1, protein kinase B (Akt), and the forkhead transcription factor FoxO1a is dose-dependently inhibited by dexadenosine (50, 100 µM). 3-Deazaadenosine (50 µM) blocks Ras signaling, which prevents the growth of vascular smooth muscle cells (VSMCs) [3].
3-Deazaadenosine exhibits potent in vitro activities across multiple biological systems. It inhibits HIV-1 replication in peripheral blood mononuclear (PBMC) cells infected with HIV-1 isolates A012 and A018, with IC50 values of 0.15 and 0.20 μM, respectively. The compound suppresses vascular smooth muscle cell (VSMC) proliferation by interfering with Ras signaling. In RAW 264.7 macrophages, 3-Deazaadenosine (1-100 μM) inhibits LPS-induced TNF-α mRNA expression in a dose-dependent manner. It also modulates NF-κB activity by enhancing nuclear translocation while blocking LPS-induced transcriptional activity, and causes proteolytic degradation of IκBα. |
| ln Vivo |
In vivo studies have demonstrated the therapeutic potential of 3-Deazaadenosine in various disease models. The compound has been shown to prevent neointima formation in a rat model of vascular injury by interfering with Ras signaling in smooth muscle cells. Its anti-inflammatory properties have been validated in immune and vascular cell models, where it suppresses inflammatory gene expression and modulates key signaling pathways. The compound also exhibits anti-proliferative effects in vivo, consistent with its ability to inhibit cell cycle progression and signaling pathways such as Ras–ERK and PI3K–Akt. However, detailed in vivo pharmacokinetic and efficacy data are limited in the available literature.
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| Enzyme Assay |
The in vitro enzyme activity assay for 3-Deazaadenosine typically measures its inhibition of S-adenosylhomocysteine hydrolase (SAHH) activity. Recombinant SAHH enzyme is incubated with varying concentrations of the test compound and its substrate, S-adenosylhomocysteine (SAH), in a suitable buffer system. The enzymatic reaction is allowed to proceed, and the production of adenosine and homocysteine is quantified, often using HPLC or a coupled enzyme assay. The inhibitor constant (Ki) is determined by analyzing the enzyme kinetics in the presence of different inhibitor concentrations, with 3-Deazaadenosine showing a Ki of 3.9 μM.
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| Cell Assay |
Cellular assays for 3-Deazaadenosine are performed in various cell lines to evaluate its anti-HIV, anti-inflammatory, and anti-proliferative activities. For anti-HIV activity, peripheral blood mononuclear (PBMC) cells are infected with HIV-1 isolates and treated with various concentrations of the compound. After several days of culture, p24 antigen levels in the supernatant are measured as an indicator of viral replication. In macrophage studies, RAW 264.7 cells are pre-treated with 3-Deazaadenosine and then stimulated with LPS. TNF-α mRNA expression is quantified by RT-PCR, and NF-κB DNA binding activity is assessed by electrophoretic mobility shift assay (EMSA).
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| Animal Protocol |
In vivo animal studies with 3-Deazaadenosine have focused on its efficacy in models of vascular injury and inflammation. In a rat model of neointima formation following vascular injury, the compound is administered systemically, and the extent of neointimal hyperplasia is assessed histologically after a defined period. The anti-inflammatory activity of 3-Deazaadenosine has also been evaluated in models of acute inflammation, where it suppresses inflammatory gene expression. However, the specific dosing regimens, routes of administration, and detailed experimental protocols are not extensively documented in the available literature and would require reference to the original research publications.
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| ADME/Pharmacokinetics |
Pharmacokinetic data for 3-Deazaadenosine indicate that it is a cell-permeable compound suitable for in vitro and in vivo studies. It is soluble in DMSO at 130 mg/mL (488.26 mM), facilitating preparation for both cellular and animal experiments. The compound is stable when stored as a powder at -20°C for up to 3 years and in solution at -80°C for up to 1 year. However, detailed pharmacokinetic parameters such as half-life, bioavailability, volume of distribution, and clearance are not extensively reported in the available literature and would require further investigation.
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| Toxicity/Toxicokinetics |
Toxicological data for 3-Deazaadenosine indicate that the compound has been used in various cell-based assays at concentrations up to 100 μM without overt toxicity in some models. In RAW 264.7 cells, treatment with 1-100 μM 3-Deazaadenosine inhibited TNF-α mRNA expression. In 3T3-L1 preadipocytes, the compound showed little toxicity at concentrations of 20-100 μM. However, comprehensive toxicology studies, including acute and chronic toxicity, genotoxicity, and target organ toxicity, have not been reported in the available literature for this research compound.
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| References |
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| Additional Infomation |
3-Deazaadenosine is a research-grade compound not approved for clinical use. Its primary value lies in its role as a pharmacological tool for studying methylation-dependent processes and as a lead compound for drug development. The compound's ability to inhibit SAHH and subsequently modulate cellular methylation makes it a valuable probe for investigating epigenetic regulation, viral replication, and inflammatory signaling. It has been cited in numerous peer-reviewed publications for its diverse biological activities, including anti-HIV, anti-inflammatory, and anti-proliferative effects.
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| Molecular Formula |
C11H14N4O4
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|---|---|
| Molecular Weight |
266.257
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| Exact Mass |
266.101
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| CAS # |
6736-58-9
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| Related CAS # |
3-Deazaadenosine hydrochloride;86583-19-9
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| PubChem CID |
23190
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| Appearance |
White to off-white solid powder
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| Density |
1.9±0.1 g/cm3
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| Boiling Point |
665.7±65.0 °C at 760 mmHg
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| Melting Point |
228-229ºC
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| Flash Point |
356.4±34.3 °C
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| Vapour Pressure |
0.0±2.1 mmHg at 25°C
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| Index of Refraction |
1.834
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| LogP |
0.18
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| Hydrogen Bond Donor Count |
4
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| Hydrogen Bond Acceptor Count |
7
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
19
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| Complexity |
334
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| Defined Atom Stereocenter Count |
4
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| SMILES |
C1=CN=C(C2=C1N(C=N2)[C@H]3[C@@H]([C@@H]([C@H](O3)CO)O)O)N
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| InChi Key |
DBZQFUNLCALWDY-PNHWDRBUSA-N
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| InChi Code |
InChI=1S/C11H14N4O4/c12-10-7-5(1-2-13-10)15(4-14-7)11-9(18)8(17)6(3-16)19-11/h1-2,4,6,8-9,11,16-18H,3H2,(H2,12,13)/t6-,8-,9-,11-/m1/s1
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| Chemical Name |
1H-Imidazo(4,5-c)pyridin-4-amine, 1-beta-D-ribofuranosyl- (9CI)
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| Synonyms |
Deaza-Ado 3-deaza- 3dAdoAdenosine3-Deazaadenosine
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| HS Tariff Code |
2934.99.9001
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| 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)
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| Solubility (In Vitro) |
DMSO : ~130 mg/mL (~488.26 mM)
H2O : ~100 mg/mL (~375.59 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.17 mg/mL (8.15 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.17 mg/mL (8.15 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 21.7 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.17 mg/mL (8.15 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.7557 mL | 18.7786 mL | 37.5573 mL | |
| 5 mM | 0.7511 mL | 3.7557 mL | 7.5115 mL | |
| 10 mM | 0.3756 mL | 1.8779 mL | 3.7557 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.
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