Vancomycin HCl CAS NO 1404-93-9 Inquire about Vancomycin HCl

Tecoland supplies Vancomycin HCl bulk active pharmaceutical ingredient (API) to the pharmaceutical industry. Our Vancomycin HCl is manufactured by cGMP compliant facility. Welcome to contact us for further details including current DMF status for the product and up to date regulatory status of the manufacturing facility. We look forward to assisting you with your research and development projects.

What is Vancomycin HCl?

Vancomycin INN is a glycopeptide antibiotic used in the prophylaxis and treatment of infections caused by Gram-positive bacteria. Vancomycin was first isolated in 1953 at Eli Lilly, from a soil sample collected from the interior jungles of Borneo by a missionary. It is a naturally occurring antibiotic made by the soil bacterium Actinobacteria species Amycolatopsis orientalis (formerly designated Nocardia orientalis). It is a complex chemical compound and an example of a comparatively rare haloorganic natural compound, containing two covalently bonded chlorine atoms.

The compound was industrially produced by fermentation and given the generic name vancomycin, derived from the term “vanquish.” The original indication for vancomycin was for the treatment of penicillin-resistant Staphylococcus aureus, a use kept alive for many years by the fact that compound had to be given intravenously and thus provided bacteria fewer opportunities to evolve resistance, and the fact that organisms were relatively slow to evolve to adapt to it, even in experiments.

For many years since its initial use, vancomycin has traditionally been reserved as a drug of “last resort”, used only after treatment with other antibiotics had failed,[citation needed]. Recently, however, vancomycin resistant organisms are becoming common. Thus, vancomycin is increasingly being displaced from this role by newer antibiotics such as linezolid (Zyvox), daptomycin (Cubicin), and quinupristin/dalfopristin (Synercid).

Indications

Vancomycin HCl is indicated for the treatment of serious, life-threatening infections by Gram-positive bacteria that are unresponsive to other less-toxic antibiotics. In particular, vancomycin should not be used to treat methicillin-sensitive Staphylococcus aureus because it is inferior to penicillins such as nafcillin.

The increasing emergence of vancomycin-resistant enterococci has resulted in the development of guidelines for use by the Centers for Disease Control (CDC) Hospital Infection Control Practices Advisory Committee. These guidelines restrict use of vancomycin to the following indications:

  • Treatment of serious infections caused by susceptible organisms resistant to penicillins (methicillin-resistant Staphylococcus aureus and multi-resistant Staphylococcus epidermidis (MRSE)) or in individuals with serious allergy to penicillins.
  • Treatment of Pseudomembranous colitis caused by the bacterium Clostridium difficile; in particular, in cases of relapse or where the infection is unresponsive to metronidazole treatment (for this indication, vancomycin is given orally, rather than via its typical, I.V. route)
  • For treatment of infections caused by gram-positive microorganisms in patients with serious allergies to beta-lactam antimicrobials.
  • Antibacterial prophylaxis for endocarditis following certain procedures in penicillin-hypersensitive individuals at high risk
  • Surgical prophylaxis for major procedures involving implantation of prostheses in institutions with a high rate of MRSA or MRSE
  • Early in treatment as an empiric antibiotic for possible MRSA infection while waiting for culture identification of the infecting organism.
What is the mechanism of action?

The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides. Normally this is a five-point interaction. This binding of vancomycin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.

Pharmacodynamics

Vancomycin is a branched tricyclic glycosylated nonribosomal peptide produced by the fermentation of the Actinobacteria species Amycolatopsis orientalis (formerly Nocardia orientalis). It is often reserved as the “drug of last resort”, used only after treatment with other antibiotics had failed. Vancomycin has been shown to be active against most strains of the following microorganisms, both in vitro and in clinical infections: Listeria monocytogenes, Streptococcus pyogenes, Streptococcus pneumoniae (including penicillin-resistant strains), Streptococcus agalactiae, Actinomyces species, and Lactobacillus species. The combination of vancomycin and an aminoglycoside acts synergistically in vitro against many strains of Staphylococcus aureus, Streptococcus bovis, enterococci, and the viridans group streptococci.

How to dose Vancomycin HCl?

Intravenous vs oral administration

Vancomycin must be given intravenously (IV) for systemic therapy, since it is not absorbed from the intestine. It is a large hydrophilic molecule that partitions poorly across the gastrointestinal mucosa. Due to short half-life it is often injected twice-daily.

The only indication for oral vancomycin therapy is in the treatment of pseudomembranous colitis, where it must be given orally to reach the site of infection in the colon. Following oral administration, the fecal concentration of vancomycin is around 500 µg/mL (sensitive strains of C. difficile have a mean inhibitory concentration of ¡Ü2 µg/mL)

Inhaled vancomycin has also been used (off-label), via nebulizer, for treatment of various infections of the upper and lower respiratory tract.

The caustic nature of vancomycin makes IV therapy using peripheral lines a risk for thrombophlebitis. Ideally, central lines, PICCs, or infusion ports should be used.

What are the side effects of Vancomycin HCl?

Although vancomycin levels are usually monitored, in an effort to reduce adverse events, the value of this is not beyond debate. Peak and trough levels are usually monitored, and, for research purposes, the area under the curve is also sometimes used. Toxicity is best monitored by looking at trough values.

Common adverse drug reactions associated with IV vancomycin include: local pain, which may be severe and/or thrombophlebitis.

Damage to the kidneys and to the hearing was a side-effect of the early impure versions of vancomycin, and these were prominent in the clinical trials conducted in the mid-1950s. Later trials using purer forms of vancomycin found that nephrotoxicity is an infrequent adverse effect, but that this is accentuated in the presence of aminoglycosides.

Rare adverse effects include: anaphylaxis, toxic epidermal necrolysis, erythema multiforme, red man syndrome, superinfection, thrombocytopenia, neutropenia, leucopenia, tinnitus, dizziness and/or ototoxicity.

It has recently been emphasized that vancomycin can induce platelet-reactive antibodies in the patient, leading to severe thrombocytopenia and bleeding with florid petechial hemorrhages, ecchymoses, and wet purpura.

Disclaimer:

Information on this page is provided for general information purposes. You should not make a clinical treatment decision based on information contained in this page without consulting other references including the package insert of the drug, textbooks and where relevant, expert opinion. We cannot be held responsible for any errors you make in administering drugs mentioned on this page, nor for use of any erroneous information contained on this page.