| Size | Price | Stock | Qty |
|---|---|---|---|
| 100mg |
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| Other Sizes |
| Targets |
2-Aminopurine has multiple targets, including double-stranded RNA-dependent protein kinase (PKR), cyclin-dependent kinase 2 (CDK2), and eukaryotic translation initiation factor 2α kinases. 2-AP inhibits PKR by competitively binding to the ATP-binding site of the kinase, thereby blocking its kinase activity. It also inhibits CDK2 through ATP-binding site interactions, affecting cell cycle regulation. Additionally, in hypothalamic cells, 2-AP inhibits leptin signal transduction at the level of the Ob-Rb leptin receptor, dose-dependently suppressing the phosphorylation of STAT3, ERK, and JNK.
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| ln Vitro |
2-Aminopurine's nucleic acid base is greatly quenched by trona when it is incorporated into an oligonucleotide, making it unavailable as a nucleic acid marker. But the precise and accurate fluorescent label for nucleic acid structures is 2-aminopurine, thanks to its extremely sensitive property to inter-base quenching [1]. 6-aminopurine differs from 2-aminopurine merely in the position outside the ring, but its fluorescence intensity is hundreds of times greater than that of purine and adenine [1].
2-Aminopurine exhibits multiple in vitro biological activities: (1) It inhibits PKR kinase activity via competitive binding to the ATP site; (2) In A549 lung cancer cells, 2-AP reverses TGF-β1-induced epithelial-mesenchymal transition (EMT), restores E-cadherin expression, inhibits fibronectin and vimentin expression, and suppresses cell metastasis; (3) It inhibits total cellular RNA and protein synthesis in a concentration-dependent manner in multiple cell lines, including C6-2B, HeLa, Swiss 3T3, and BALB/c cells. |
| ln Vivo |
In vivo activity of 2-Aminopurine has been demonstrated in various animal models. In a mouse model of pulmonary fibrosis, 2-AP treatment significantly reduced bleomycin-induced pulmonary inflammation, EMT, and fibrosis, along with decreased mortality. In a sepsis mouse model, 2-AP alleviated organ dysfunction and reduced plasma inflammatory factor levels. In an ApoE-/- mouse atherosclerosis model, oral administration of 200 mg/kg once every other day for 30 days significantly reduced atherosclerotic plaque area. In a Chagas disease mouse model, 2-AP improved cardiac pathology by inhibiting ER stress and reduced ventricular enlargement. The antiviral prodrug derivative APD was safe in a woodchuck model of chronic HBV infection, producing dose-dependent reductions in serum WHV viremia following 4 weeks of oral administration.
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| Enzyme Assay |
In vitro enzyme assays typically employ 2-aminopurine's fluorescence properties. For PKR kinase inhibition assays, experiments are conducted in buffer containing [γ-³²P]ATP, with recombinant PKR and substrates (e.g., histones) incubated with various concentrations of 2-AP. Phosphorylation levels are detected by autoradiography, and double-reciprocal plots are used to analyze competitive inhibition with respect to ATP. For nucleic acid interaction studies, 2-AP fluorophores are incorporated into specific sites of oligonucleotides (e.g., hairpins or mismatch sites). Fluorescence changes are monitored in real time using a fluorescence spectrophotometer, with excitation/emission wavelengths typically at 313/350 nm (or 320/381 nm), measuring emission around 370 nm.
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| Cell Assay |
A typical in vitro cell experiment procedure involves culturing target cells (e.g., HEK293, A549, HeLa, PC12, or V79 cells) in DMEM or RPMI 1640 medium supplemented with 10% fetal bovine serum at 37°C in 5% CO₂ until the logarithmic growth phase. 2-Aminopurine treatment (ranging from 1 μM to 5 mM) is initiated 24 hours after cell seeding. For RNA and protein synthesis inhibition studies, 2-AP is added within the first 4 hours to observe concentration-dependent effects. Cells are treated for 18–40 hours, after which cell lysates are collected for immunoblotting, RNA extraction for quantitative real-time PCR, or flow cytometry for cell cycle analysis.
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| Animal Protocol |
In vivo experiments are typically conducted in rodent models, including C57BL/6 mice, ApoE knockout mice, and Wistar rats. Animals are acclimated for one week prior to dosing and randomly divided into control and 2-AP treatment groups. 2-AP is administered by oral gavage every other day at doses ranging from 200 to 400 mg/kg body weight for 30 days. In sepsis models, the cecal ligation puncture method is used to establish the model, and serum is collected 24 hours post-operation for detection of ALT, AST, Cr, BUN, and inflammatory cytokines. Endpoints typically include survival observation, histopathological examination, serum biochemical analysis, and target tissue protein expression detection (e.g., Western blot for phosphorylated proteins).
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| ADME/Pharmacokinetics |
Direct systemic pharmacokinetic data for 2-Aminopurine are limited; most information is derived from studies of its prodrug derivative APD. In a woodchuck model, APD is efficiently converted to the active metabolite DXG after oral administration, with higher serum concentrations of DXG following oral versus intravenous administration, indicating significant first-pass intestinal and/or hepatic metabolism. Oral administration of APD (1, 3, 10, 30 mg/kg) produced dose-dependent antiviral responses characterized by reductions in serum WHV viremia. A related analog, Cyclo-D4G, in rats showed an elimination half-life of 0.78±0.14 h after intravenous administration and 0.83±0.13 h after oral administration, with an oral bioavailability of 26.9%.
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| Toxicity/Toxicokinetics |
2-Aminopurine is classified as harmful. Acute toxicity data show oral LD₅₀ (rat) of 723 mg/kg and intraperitoneal LD₅₀ (rat) of 270 mg/kg. Mouse toxicological studies demonstrated that the 400 mg/kg dose group of 2-AP resulted in 100% mortality within 14 days, with undigested food accumulation in the stomach but no significant pathological changes in other organs. The 300 mg/kg dose retarded growth without causing death, while doses of 200 mg/kg or lower once every other day did not reduce food intake, alter serum glucose levels or body weight, or increase mortality, and can be used for mouse treatment without detectable adverse effects. Hazard statements include harmful if swallowed (H302), causes skin irritation (H315), and causes serious eye irritation (H319). This compound exhibits weak mutagenic activity in vitro but is inactive as a carcinogen in
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| References |
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| Additional Infomation |
2-Aminopurine is the parent compound of the 2-aminopurine class of compounds, consisting of a purine core and an amino substituent at the 2-position. It is an antimetabolite. It is a member of the 2-aminopurine class of compounds and also a nucleobase analog. It is an isomer of adenine (6-aminopurine).
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| Molecular Formula |
C5H5N5
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|---|---|
| Molecular Weight |
135.1267
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| Exact Mass |
135.054
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| CAS # |
452-06-2
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| Related CAS # |
2-Aminopurine dihydrochloride;1428126-74-2
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| PubChem CID |
9955
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| Appearance |
Light yellow to yellow solid powder
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| Density |
1.9±0.1 g/cm3
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| Boiling Point |
328.2±25.0 °C at 760 mmHg
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| Melting Point |
280-282 °C(lit.)
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| Flash Point |
152.3±23.2 °C
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| Vapour Pressure |
0.0±0.7 mmHg at 25°C
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| Index of Refraction |
1.954
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| LogP |
-1.33
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| Hydrogen Bond Donor Count |
2
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| Hydrogen Bond Acceptor Count |
4
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| Rotatable Bond Count |
0
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| Heavy Atom Count |
10
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| Complexity |
127
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
MWBWWFOAEOYUST-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C5H5N5/c6-5-7-1-3-4(10-5)9-2-8-3/h1-2H,(H3,6,7,8,9,10)
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| Chemical Name |
7H-purin-2-amine
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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 Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| 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 : ~5 mg/mL (~37.00 mM)
H2O : ~1.35 mg/mL (~9.99 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: 2.5 mg/mL (18.50 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication (<60°C).
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 7.4003 mL | 37.0014 mL | 74.0028 mL | |
| 5 mM | 1.4801 mL | 7.4003 mL | 14.8006 mL | |
| 10 mM | 0.7400 mL | 3.7001 mL | 7.4003 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.
| NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
| NCT06210750 | WITHDRAWN | Procedure: Biospecimen Collection Procedure: Bone Marrow Aspiration Procedure: Bone Marrow Biopsy |
T Acute Lymphoblastic Leukemia T Lymphoblastic Lymphoma |
National Cancer Institute (NCI) | 2024-08-09 | Phase 2 |
| NCT02521493 | ACTIVE, NOT RECRUITING | Drug: Asparaginase Drug: Asparaginase Erwinia chrysanthemi Drug: Cytarabine |
Acute Myeloid Leukemia Down Syndrome Myelodysplastic Syndrome Myeloid Leukemia Associated With Down Syndrome Myeloproliferative Neoplasm |
Children's Oncology Group | 2015-12-23 | Phase 3 |
| NCT04546399 | SUSPENDED | Radiation: 3-Dimensional Conformal Radiation Therapy Biological: Blinatumomab Drug: Cyclophosphamide |
Down Syndrome Recurrent B Acute Lymphoblastic Leukemia |
National Cancer Institute (NCI) | 2020-12-04 | Phase 2 |
| NCT03007147 | ACTIVE, NOT RECRUITING | Procedure: Allogeneic Hematopoietic Stem Cell Transplantation Drug: Calaspargase Pegol Drug: Cyclophosphamide |
Acute Lymphoblastic Leukemia B Acute Lymphoblastic Leukemia Mixed Phenotype Acute Leukemia T Acute Lymphoblastic Leukemia |
Children's Oncology Group | 2017-08-08 | Phase 3 |
| NCT06317662 | NOT YET RECRUITING | Drug: Asparaginase Erwinia chrysanthemi Procedure: Biospecimen Collection Biological: Blinatumomab |
Acute Leukemia of Ambiguous Lineage B Acute Lymphoblastic Leukemia |
National Cancer Institute (NCI) | 2024-10-28 | Phase 2 |
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