2-5A
2-5A (2′,5′-ApApA) is a 5'-triphosphorylated (2',5') oligoadenylate. When covalently linked to an antisense molecule complementary to the target sequence, 2-5A activates RNase L, which subsequently degrades the target RNA bound to the 2-5A chimera. 2-5A can be used in research related to respiratory syncytial virus infection, colorectal adenocarcinoma and melanoma.
For research use only. We do not sell to patients.
- CAS No.: 65954-93-0
- Formula: C30H40N15O25P5
- Molecular Weight:1165.59
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
All DNA/RNA Synthesis Isoforms
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Biological Activity
Description
IC50 & Target
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RNASE L |
In Vitro
2-5A (1 μM; 4 h) is imported by human HEK293T cells and BJ1 fibroblasts to activate RNase L-dependent IFN/ISG induction, while mouse MEFs, MC38 cells, BMDMs, human A549 cells, and THP-1 monocytes do not exhibit robust 2-5A import activity[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:human HEK293T cells, human BJ1 fibroblasts, mouse MEFs, mouse MC38 cells, mouse bone-marrow-derived macrophages (BMDMs), human A549 cells, human THP-1 monocytes
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Concentration:1 μM
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Incubation Time:4 h
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Result:Stimulated significant IFNB1 and CXCL10 mRNA expression in human HEK293T cells and BJ1 fibroblasts.
Abolished IFN/ISG response in RNase L-knockout HEK293T and BJ1 cells.
Failed to induce robust IFN/ISG response in mouse MEFs, MC38 cells, BMDMs, human A549 cells, and THP-1 monocytes.
Induced robust IFN/ISG expression in all tested cell lines when transfected with Lipofectamine.
In Vivo
2-5A (10 μg; peritumoral injection; once daily; 3 consecutive days) complexed with lipofectamine significantly inhibits B16 melanoma tumor growth in wild-type C57BL/6J mice[3].
2-5A (10 μg; peritumoral injection; once daily; 3 consecutive days) complexed with lipofectamine significantly inhibits sgRnasel MC38 colorectal carcinoma tumor growth in wild-type C57BL/6J mice[3].
2-5A (10 μg; peritumoral injection; once daily; 3 consecutive days) complexed with lipofectamine does not inhibit MC38 colorectal carcinoma tumor growth in RnaseI−/− mice[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J wild-type (6-8 weeks old, same sex, subcutaneous implantation of 5×105 WT MC38 cells)[3]
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Dosage:10 μg (complexed with lipofectamine)
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Administration:peritumoral injection; once daily; 3 consecutive days
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Result:Significantly inhibited MC38 tumor growth compared to PBS, naked 2-5A (TEA), or lipofectamine alone.
Showed statistically significant difference in tumor volume between the lipofectamine+2-5A group and lipofectamine alone group (P=0.0142).
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Animal Model:C57BL/6J wild-type (6-8 weeks old, same sex, subcutaneous implantation of 5×105 B16 cells)[3]
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Dosage:10 μg (complexed with lipofectamine)
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Administration:peritumoral injection; once daily; 3 consecutive days
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Result:Significantly inhibited B16 melanoma tumor growth compared to lipofectamine alone (P=0.0185).
Chemical Information
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CAS No. 65954-93-0
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Molecular Weight 1165.59
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Formula C30H40N15O25P5
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SMILES
NC1=NC=NC2=C1N=CN2[C@H]3[C@H](OP(O)(OC[C@@H](O[C@H]([C@@H]4OP(O)(OC[C@@H](O[C@H]([C@@H]5O)N6C=NC7=C6N=CN=C7N)[C@H]5O)=O)N8C=NC9=C8N=CN=C9N)[C@H]4O)=O)[C@H](O)[C@@H](COP(OP(OP(O)(O)=O)(O)=O)(O)=O)O3
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Synonyms
2′,5′-ApApA; 2′,5′-trioligoadenylate; 5'-O-Triphosphoryladenylyl-(2'→5')-adenylyl-(2'→5')-adenosine
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
References
[1]. Barnard DL, et al. 2-5A-DNA conjugate inhibition of respiratory syncytial virus replication: effects of oligonucleotide structure modifications and RNA target site selection. Antiviral research. 1999 Apr;41(3):119-34. [Content Brief]
[2]. Wang S, et al. 2-5A is an immunotransmitter that fuels RNase L immunity. Immunity. 2025 Apr 08;58(4):770-772. [Content Brief]
[3]. Huai W, et al. OAS cross-activates RNase L intercellularly through cell-to-cell transfer of 2-5A to spread innate immunity. Immunity. 2025 Apr 08;58(4):797-810.e6. [Content Brief]
[4]. Kalinichenko EN, et al. 3'-Fluoro-3'-deoxy analogs of 2-5A 5'-monophosphate: binding to 2-5A-dependent endoribonuclease and susceptibility to (2'-5')phosphodiesterase degradation. Biochemical and biophysical research communications. 1990 Feb 28;167(1):20-6. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
2-5A Related Classifications
HY-173189 Related Classifications
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Keywords
- 2-5A
- 65954-93-0
- 2′,5′-ApApA
- 2′,5′-trioligoadenylate
- 5'-O-Triphosphoryladenylyl-(2'→5')-adenylyl-(2'→5')-adenosine
- RSV
- DNA/RNA Synthesis
- RNase L
- Sendai virus
- HEK293T human embryonic kidney cells
- BJ1 human foreskin fibroblasts
- ENPP1
- MC38 cells
- melanoma
- vesicular stomatitis virus
- colorectal adenocarcinoma
- respiratory syncytial virus
- Inhibitor
- inhibitor
- inhibit