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Tweaking The Immune System Can Help Fight Cancer & Block Angiogenesis

  
  
  
angiogenesis

Cancers that become resistant to an important class of drugs might be made vulnerable by tweaking the immune system, a team led by UCSD researcher Napolene Ferrara has found.

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G-418 FAQS (Frequently Asked Questions)

  
  
  
G418 resized 600

For the last 15 years, A.G. Scientific has been a leading manufacturer, and supplier of g-418, Geneticin®.  Our success with a combination of fermentation & synthesis that has allowed us to build a catalog of over 160 antibiotics and a customer base of researchers, catalog biochemical distributors and cell media manufacturers worldwide. Click here for our Comprehensive Antibiotic E-Guide. We offer the full range of services: custom bottling, sterile formulations, custom packaging, as well as, a full suite of private labeling capabilities.   

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29 RAPAMYCIN IMMUNOSUPPRESSANT FACTS

  
  
  
rapamycin

Background Information

 

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Treating Cancer Using Epirubicidin

  
  
  
epirubicidin, anthracycline, antibiotics, anticancer

MECHANISM OF ACTIONThe mechanism of action of epirubicin appears to be related to its ability to bind to nucleic acids. It forms a complex with DNA by intercalation between base pairs, resulting in inhibition of DNA and RNA synthesis. Intercalation also triggers DNA cleavage by topoisomerase II, resulting in cytocidal activity. Binding to cell membranes and plasma proteins may also be involved. Epirubicin also generates cytotoxic free radicals. Epirubicin is the 4’-epimer of DOXOrubicin; i.e., there is a different spatial orientation of the hydroxyl group at the 4’ carbon of the sugar moiety. This difference may account for faster elimination and reduced toxicity.

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Benzoquinonoid Ansamycins Antibiotics

  
  
  
Representative benzoquinoid antibiotics  resized 600

Ansamycins is a family of secondary metabolites that show antimicrobial activity against many gram-positive and some gram-negative bacteria and includes various compounds, among which: streptovaricins and rifamycins. In addition, these compounds demonstrate antiviral activity towards bacteriophages and poxviruses.

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Paclitaxel - A Mitotic Inhibitor Used in Cancer Chemotherapy

  
  
  
P 1027, 3d structure
  • CAS #: 33069-62-4
  • Chemical Name: Taxol, Baccatin III N-benzyl-β-phenylisoserine ester
  • Chemical Formula: C47H51NO14
  • Appearance: White Crystalline Powder
  • Merck Index: 12.7117.1996
  • Molecular Weight: 853.9
  • Solubility: Soluble in DMSO, Ethanol, Methanol; Clear colorless solution at 10 mg/ml DMSO and 10 mg/ml methanol
  • Storage Temp: -20°C
  • Melting Point: 215-217°C

Paclitaxel, Taxus brevifolia, commonly known as the Pacific yew, is a member of the yew family (Taxaceae). It is a small, slow growing evergreen tree native to the northwestern United States (Wheeler et al., 1992). In 1971, a natural product called taxol that was isolated from T. brevifolia. Taxol has been found to be a mitotic inhibitor used for cancer chemotherapy.

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Piperlonguminine: Potential Treatment For Alzheimer's Disease

  
  
  
piper longum, long pepper, piperlonguminine, alzheimer's treatment, alzheimers, antimicrobial, antitumor, anticancer, amyloid, bacillus subtilis, candida tropicalis, cancer research

Piperlonguminine is a potential novel therapeutic agent for Alzheimer’s disease.  Extracellular deposits of Aβ in senile plaques of the cerebral cortex are known to be hallmarks of Alzheimer’s disease.  Recent studies show that a mix of piperlonguminine and dihydropiperlonguminine significantly inhibit the expression of Amyloid Precursor Protein (APP).  The decreased production of the peptide Amyloid β (Aβ) in SK-N-SH cells is a beneficial effect to Alzheimer’s Disease.

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Chemotin and HIF-1

  
  
  
HIF-1. HIF-2, chetomin,immunosuppressive,antifungal,anticancer,IMMUNOSUPPRESANT

Hypoxia-inducible factor-1 (HIF-1) is a transcriptional complex that is activated in response to hypoxia and growth factors. HIF-1 plays a central role in tumor progression, invasion, and metastasis. Overexpression of the HIF-1α subunit has been observed in many human cancers and is associated with a poor prognostic outcome with conventional treatments. Targeting HIF-1 using novel small molecule inhibitors is, therefore, an attractive strategy for therapeutic development.

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Cycloheximide-induced T-cell Death Is Mediated by a Fas-associated Death Domain-dependent Mechanism

  
  
  
biochemicals,BIOMEDICAL RESEARCH,MOLECULAR BIOLOGY,CELL BIOLOGY,biotech,BIOTECHNOLOGY,bioproduction,apoptosis,biology,biochemical, actidione

Cycloheximide (CHX) can contribute to apoptotic processes, either in conjunction with another agent (e.g. tumor necrosis factor-α) or on its own. The apoptotic process is now known to involve the well orchestrated interactions of cell death receptors, death receptor adaptors, caspases, and Bcl-2 family members. Although a number of stimuli have been reported to result in the up-regulation of the Fas receptor and its ligand (e.g. UV, c-Myc, and certain chemotherapeutic drugs), there are many other stimuli for which the mechanism responsible for their action is still unknown. An example of the latter is the ability of cycloheximide (CHX) to either promote or inhibit apoptosis in divergent cell types and in response to varying death stimuli. A large body of evidence has shown that CHX can potentiate, and in some cases (e.g. TNFα stimulation and staurosporine) be necessary for, the apoptotic effects of certain death stimuli. The studies of Martin et al. and Tuschida et al. further indicated that CHX, independently of other stimuli, is also capable of promoting apoptosis in a number of transformed cell lines and normal cells. Jacobsonet al. has shown that staurosporine- and staurosporine/cycloheximide-induced death is mediated by a caspase-3-like activity that is blocked by Z-VAD-FMK, a synthetic tripeptide inhibitor that demonstrates broad caspase specificity. More recently, Woo et al. demonstrated that bone marrow neutrophils from caspase-3−/− mice no longer undergo CHX-induced apoptosis, indicating that caspase-3 expression is most likely required for this type of cell death.

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