Puromycin aminonucleoside
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| Category | Antibiotics |
| Catalog number | BBF-04561 |
| CAS | 58-60-6 |
| Molecular Weight | 294.31 |
| Molecular Formula | C12H18N6O3 |
| Purity | ≥95% |
Ordering Information
| Catalog Number | Size | Price | Stock | Quantity |
|---|---|---|---|---|
| BBF-04561 | 100 mg | $439 | In stock |
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Add to cartDescription
Puromycin aminonucleoside is the aminonucleoside portion of the antibiotic puromycin, which is a puromycin analogue which does not inhibit protein synthesis or induce apoptosis. It is an aminoglycoside antibiotic with anti-tumor properties.
Specification
| Synonyms | 3'-Amino-3'-deoxy-N6,N6-dimethyladenosine; 3'-Amino-3'-deoxy-N,N-dimethyladenosine; 6-(Dimethylamino)-9-(3-amino-3-deoxy-β-D-ribofuranosyl)purine; 6-Dimethylamino-9-(3-amino-3-deoxyribosyl)purine; 9-(3-Amino-3-deoxy-β-D-ribofuranosyl)-6-(dimethylamino)-9H-purine; Aminonucleoside Puromycin; NSC 3056; PANS; SAN; Stylomycin Aminonucleoside |
| Storage | Store at -20°C |
| IUPAC Name | (2R,3R,4S,5S)-4-amino-2-[6-(dimethylamino)purin-9-yl]-5-(hydroxymethyl)oxolan-3-ol |
| Canonical SMILES | CN(C)C1=NC=NC2=C1N=CN2C3C(C(C(O3)CO)N)O |
| InChI | InChI=1S/C12H18N6O3/c1-17(2)10-8-11(15-4-14-10)18(5-16-8)12-9(20)7(13)6(3-19)21-12/h4-7,9,12,19-20H,3,13H2,1-2H3/t6-,7-,9-,12-/m1/s1 |
| InChI Key | RYSMHWILUNYBFW-GRIPGOBMSA-N |
| Source | Semi-synthetic |
Properties
| Appearance | White Powder |
| Antibiotic Activity Spectrum | Neoplastics (Tumor) |
| Boiling Point | 595.6°C at 760 mmHg |
| Melting Point | 235°C (dec.) |
| Density | 1.7 g/cm3 |
| Solubility | Soluble in Ethanol, Methanol, DMF, DMSO, Water |
Reference Reading
1.Puromycin aminonucleoside increases podocyte permeability by modulating ZO-1 in an oxidative stress-dependent manner.
Ha TS1, Park HY2, Seong SB2, Ahn HY3. Exp Cell Res. 2016 Jan 1;340(1):139-49. doi: 10.1016/j.yexcr.2015.12.001. Epub 2015 Dec 9.
Puromycin aminonucleoside (PAN)-induced nephrosis is a widely studied animal model of human idiopathic nephrotic syndrome because PAN injection into rats results in increased glomerular permeability with the characteristic ultrastructural changes in podocytes similar to human nephrosis. To investigate the role of zonula occludens (ZO)-1 and oxidative stress on PAN-induced podocyte phenotypical changes and hyperpermeability in vitro, we cultured rat and mouse podocytes and treated with various concentrations of PAN. PAN treatment increased oxidative stress level of podocytes significantly with the induction of Nox4. In addition, PAN changed the ultrastructure of podocytes, such as shortening and fusion of microvilli, and the separation of intercellular gaps, which were improved by anti-oxidative vitamin C and Nox4 siRNA. PAN also disrupted the intercellular linear ZO-1 staining and induced inner cytoplasmic re-localization of ZO-1 protein, resulting in increased podocyte intercellular permeability.
2.A vital role for myosin-9 in puromycin aminonucleoside-induced podocyte injury by affecting actin cytoskeleton.
Yuan Y1, Zhao C1, An X2, Wu L1, Wang H1, Zhao M3, Bai M3, Duan S1, Zhang B1, Zhang A3,4, Xing C1. Free Radic Res. 2016 Mar 31:1-11. [Epub ahead of print]
Podocyte injury is an early pathological change of many kidney diseases. In particular, the actin cytoskeleton plays an important role in maintaining the normal function of podocytes. Disruption of the actin cytoskeleton is a feature of podocyte injury in proteinuric nephropathies. Recent studies showed that myosin-9 was localized in the podocyte foot processes and was necessary in maintaining podocyte structural homeostasis. However, it is unclear whether myosin-9 maintains podocyte structure by affecting actin cytoskleton. Here, the role of myosin-9 in puromycin aminonucleoside (PAN)-induced podocyte injury was explored both in vitro and in vivo. In cultured mouse podocytes (MPC5), it was determined that PAN downregulated myosin-9 expression, disrupted the actin cytoskeleton and reduced the adhesion ability. Reduced myosin-9 expression by siRNA precipitated podocyte cytoskeletal damage and accelerated PAN-induced podocyte detachment. Overexpression of myosin-9 protected against PAN-induced podocyte detachment.
3.Effect of clofibrate on fatty acid metabolism in the kidney of puromycin-induced nephrotic rats.
Muroya Y1, Ito O2. Clin Exp Nephrol. 2016 Mar 7. [Epub ahead of print]
BACKGROUND: Proteinuria plays an essential role in the progression of tubulointerstitial damage, which causes end-stage renal disease. An increased load of fatty acids bound to albumin reabsorbed into proximal tubular epithelial cells (PTECs) contributes to tubulointerstitial damage. Fibrates, agonists of peroxisome proliferator-activated receptor α (PPARα), have renoprotective effects against proteinuria whereas the effects of these compounds on fatty acid metabolism in the kidney are still unknown. Therefore, the present study examined whether the renoprotective effects of clofibrate were associated with improvement of fatty acid metabolism in puromycin aminonucleoside (PAN)-induced nephrotic rats.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
