Aklavin
Aklavin is a structural analog of Aclacinomycin A (HY-N2306) produced by Streptomyces strain A 1165. Aklavin possesses Z-DNA-inducing and stabilizing activities, along with antibiotic, anti-phage and broad-spectrum antimicrobial activities. Aklavin inhibits the proliferation of various viruses (such as influenza virus and poliovirus) and interferes with their nucleoprotein synthesis, while also exhibiting inhibitory effects on staphylococci, mycobacteria and specific fungi. Aklavin blocks phage-induced bacterial lysis by regulating host-parasite interactions. Aklavin shows specific toxicity to fertilized eggs and mice, and does not alter the splicing of the SMN2 gene.
For research use only. We do not sell to patients.
- CAS No.: 60504-57-6
- Formula: C30H35NO10
- Molecular Weight:569.60
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
In Vitro
Aklavin (0.001-5.0 mg/mL) shows variable phagocidal activity against free phage particles, with paratyphoid Poona phage 1 being the most sensitive (99% inactivation at 0.05 mg/mL) and Bacillus cereus phage being the least sensitive (33% inactivation at 5.0 mg/mL), and requires far higher concentrations to inactivate free phages than to prevent phage-mediated lysis[2].
Aklavin (24 h; 72 h) inhibits bacterial growth with varying potency via agar dilution assay, showing the highest potency against Corynebacterium sepedonicum (minimum inhibitory concentration 1.56 μg/mL after 72 hr incubation) and the lowest potency against 7 bacterial species (minimum inhibitory concentration >100 μg/mL after 24 hr incubation)[2].
Aklavin hydrochloride (0.1-10 nM; 5 days) does not alter the SMN2 splicing pattern in SV40-transformed type I SMA fibroblast cell line 3061[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:SV40-transformed type I SMA fibroblast cell line 3061
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Concentration:0.1 nM, 1 nM, 10 nM
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Incubation Time:5 days
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Result:Failed to alter the SMN2 splicing pattern.
Remained comparable to untreated or DMSO-treated cells in full-length SMN transcript levels and the ratio of full-length to Δexon 7 isoforms.
In Vivo
Aklavin (0.002-0.05 mg/kg; i.p.) does not inhibit herpetic infection in mice[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mice with Eastern equine encephalomyelitis[2]
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Dosage:0.002 mg/mL, 0.01 mg/mL, 0.1 mg/mL, 1.0 mg/mL
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Administration:injection; post 1-hour pre-incubation with virus
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Result:Protected all six mice from 0.1% virus when dosed at 0.01 mg/mL, 0.1 mg/mL, or 1.0 mg/mL.
Resulted in 1 survivor out of six mice from 0.1% virus when dosed at 0.002 mg/mL.
Protected all six mice from 1% virus when dosed at 1.0 mg/mL.
Resulted in 1 survivor out of six mice from 1% virus when dosed at 0.1 mg/mL.
Resulted in 3 survivors out of six mice from 1% virus when dosed at 0.01 mg/mL.
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Animal Model:Mice with Herpetic infection[2]
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Dosage:0.002 mg/kg, 0.05 mg/kg
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Administration:i.p.
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Result:Showed no effect on herpetic infection in mice at 0.002 mg/kg dose.
Showed no effect on herpetic infection in mice at 0.05 mg/kg dose.
Chemical Information
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CAS No. 60504-57-6
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Molecular Weight 569.60
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Formula C30H35NO10
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SMILES
COC([C@@H]1C2=C(C(O)=C3C(C(C4=CC=CC(O)=C4C3=O)=O)=C2)[C@H](C[C@]1(O)CC)O[C@H]5C[C@@H]([C@@H]([C@@H](O5)C)O)N(C)C)=O
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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.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Aklavin Related Classifications
HY-121473 Related Classifications
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