 |
|
To resist antimicrobial agents (bacteria, viruses, parasites or fungi), various pathogenic microorganisms, as well as antibiotics, particularly antifungal agents, multidrug-resistant (MDR), multidrug resistance, anti-viral drugs, anthelmintic agent is a multi-state or enable a wide variety of chemicals structure and function to remove the body. Recognizing the different levels of MDR, (PDR) pandrug tolerance conditions have been introduced and extensively drug-resistant (XDR). Published in 2011 in a magazine called "infectious diseases and clinical microbiology", this article can be accessed openly, rather than describes the multi-drug resistant bacteria, fungi, viruses, parasites, definition, anti-tumor resistance is that of the tumor cells are described in the section. For animals and human therapy, leading to the selection of resistant pathogens for multiple drugs large quantities of antibiotics used for fish in aquaculture further. A plurality of resistors in the bacteria, can be generated by one of two mechanisms. First, these bacteria, can be in the same cell, each of which collect multiple genes encoding resistance to the drug. The (R), usually, this accumulation occurs plasmids impedance. Second, multi-drug resistance can occur by increased expression of genes extrusion a wide range of drugs, encoding the efflux pump more than one. This review describes our current knowledge of the molecular mechanisms involved in both types of resistance.
Tuberculosis is an example of bacteria that are resistant to multiple drugs. Multidrug-resistant tuberculosis (MDR-TB) is defined as tuberculosis that is resistant to the most powerful first-line treatment of two and isoniazid (INH) rifampicin (RMP), for tuberculosis at least. Resistant, but not a combination of any of several other agents for INH RMP tuberculosis isolates is not classified as MDR-TB. The MDR-TB, course of antibiotics is interrupted, drug concentration in the body, is not sufficient to kill 100% of bacteria, but it has developed into treatable TB that it is not so. Sometimes may stop the course of the antibiotic and feel good, the supply of drugs is insufficient, or to become a shortage of patients can occur for several reasons, this is, at any time the patient to obtain effective treatment there is forget or you will take the medicine to the patient. TB treatment Most are composed of chemotherapy treatment of short-term course is a small percentage of patients with multidrug-resistant tuberculosis. MDR TB delay of second-line drugs is to treat difficult. MDR-TB is spread from person to person as easily in the same way as drug-sensitive tuberculosis. But, still high from the patent medicine of anti-TB price of the second line, it is a major problem for patients living in poor countries to be treated. In untreated patients, the incidence of tuberculosis is a problem in poor countries. To cure infectious diseases such as tuberculosis completely, we plan to ensure equal access to medical care is required.
Industry Challenges & Clinical Status
There is a very strong correlation between the expression of MDR-1 gene in the tumor cells or many strains derived from multi-drug resistant patients and shown by these cells. However, I will occur in cells multidrug resistance also MDR-18, does not show this correlation. This is another in cancer cells that need to be characterized in that it comprises those based on the purpose of the MRP and MDR-1, belonging to the MRP protein superfamily and MDR -1 represents a major challenge in the development of therapies actually the molecular induction of multidrug resistance, probably. The MRP-1 Beauty chemoprevention MDR, problem is that it has a normal function of cells throughout the body in this respect. They are part of the defense mechanism of the body against the toxic small molecules, and is an important player of the normal functioning liver and pump and membrane transport other body, kidney, gastrointestal gland, adrenal glands, the blood-brain barrier together. Therefore, all approaches the target, which it may not to interfere with the normal functions of these molecules in normal cells, so the method and woven cancer-specific and / or these molecules. Finally, given the correlation of the plurality that exists between the MRP and P-gp expression and the expression of other proteins in cancer cells, another issue is excellent to enable the rapid analysis of these relationships in a meaningful way it is to find a cellular model was. Yeast is a network of genes that provide phenotypic drug resistance similar to the mammalian model system cells and excellent were found. This system is widely expressed, resistance imparting agent is effective against them, are used to study the functional aspects of the membrane pump.
The Future
The P-glycoprotein MDR proteins, and those that can be used to remove a wide variety of anti-cancer compounds in the interior of the tumor cells, but recent research indicates that it is not possible for them to remove all of them are. For example, for cells exhibiting a phenotype of resistance MDR-1 mediated, novel derivatives olivacine who S16020-2 labeled, showed significant antitumor activity in in vivo and in vitro. This may be due to the higher absorption rate of the compound surrounding the P-glycoprotein leading to efficacy and high intracellular accumulation effectively. Potential customers of the other with the activity profile similar to cancer multidrug resistance, efforts to implement high-throughput screening to find them likely to be resistance and there. As the expression of mutant p53 such important development should be noted future of multidrug resistance mediated MRP and MDR-1 is, confirm the link between the mechanism and the other of these proteins for cancer We are concerned with the stand. Recent studies, in some cells, such as small cell lung such that there is a correlation between the expression of mutant p53 that can be used for prediction and MRP are shown. Such rate many other, it changes the anti-cancer agent, pharmacological genomics, the multidrug resistance of cancer which can be optionally be located either gene family these in the context it is clear there is a potential importance of them. Further, the structure Recent studies have begun to show the components of the actual MRP required for its function. This work, thereby, inactivation, will pave the way for agents that target the functional areas of these molecules specifically them. Things like that are already working. For example, MDR-1 is analyzed by being an inhibitor of the molecule substrates and wide good and / or are assumed to compare the National Cancer Institute, NCI, a program for identifying the vehicle in the database that. The future of MDR, increase profits will show a new genetic approach as a transcriptional decoy. For example, in a recent report, it indicates a method which is effective in causing leukemia cells with high resistance to vinblastine orientation of the promoter of the human MDR1 gene by antisense is susceptible to agent16 anti-cancer. In addition to these approaches, biological synthesis or combinatorial chemistry to develop a peptide or anti-cancer compounds to target regulatory sequences MDR1, blocking its expression. Finally, new molecules that may inhibit the MDR may come from different sources, and in the future, I will look at the increase in the screening of compounds from a variety of options for this purpose. For example, in a recent study, well, this is anti-fungal antibiotic Oreoba explain to you may be an important addition to the arsenal of MDR1 inhibitor also be effective inhibitors of MDR1, P-glycoprotein .
GENTAUR Belgium BVBA BE0473327336 Voortstraat 49, 1910 Kampenhout BELGIUM Tel 0032 16 58 90 45 Fax 0032 16 50 90 45 info@gentaur.com GENTAUR Ltd. GB111298832 Howard Frank Turnberry House 1404-1410 High Road Whetstone London N20 9BH Tel 020 3393 8531 Fax 020 8445 9411 |
GENTAUR France SARL FR63484237888 9, rue Lagrange, 75005 Paris Tel 01 43 25 01 50 Fax 01 43 25 01 60 RCS Paris B 484 237 888 SIRET 48423788800017 RIB 30004 00187 00010092253 10 BNP PARIBAS PARIS PL MAUBERT BIC BNPAFRPPPRG IBAN FR76 3000 4001 8700 0100 9225 310 france@gentaur.com |
GENTAUR GmbH DE815175831 Marienbongard 20 52062 Aachen Deutschland de@gentaur.com Tel 0241 95 78 94 78 Tacka Vancheva Tel logistics 0241 4008 9086 Annick Verdeyen Fax 0241 55 91 05 36 Bankleitzahl 39050000 IBAN DE8839050000107569353 Handelsregister Aachen HRB16058 Steuernummer 201/5961/3925 de@gentaur.com |
GENTAUR Nederland BV NL850396268B01 Kuiper 1 5521 DG Eersel Nederland KVK nummer 52327027 Tel: 0208-080893 Fax: 0497-517897 nl@gentaur.com IBAN: NL04RABO0156985462 SWIFT RABONL2U GENTAUR Ltd. GB111298832 Howard Frank Turnberry House 1404-1410 High Road Whetstone London N20 9BH Tel 020 3393 8531 Fax 020 8445 9411 |
GENTAUR U.S.A Genprice Inc, Logistics 547, Yurok Circle San Jose, CA 95123 Phone: (408) 472-2934 Fax:(408) 416-3994 Phone (718)513-2983 sales@genprice.com Genprice Inc, Invoices and accounting 6017 Snell Ave San Jose, CA 95123 |
GENTAUR Italy 20135 Milano Tel 0236006593 Fax 0350085071 italia@gentaur.com GENTAUR Spain tel:0911876558 spain@gentaur.com GENTAUR BULGARIA BG20135893153, Graf Ignatiev Str. ent.V, fl. 2 Sofia 1000 Tel 0035929830070 Fax 0035929830072 sofia@gentaur.com |
ГЕНТАУЪР БЪЛГАРИЯ ID # 201 358 931 BULSTAT София 1000 ул. "Граф Игнатиев" 53 вх. В, ет. 2 Tel 0035929830070 Fax 0035929830072 e-mail: Sofia@gentaur.com IBAN: BG11FINV91501014771636 BIC: FINVBGSF |
Other countries Österreich +43720880899 Canada Montreal +15149077481 Ceská republika Praha +420246019719 Danmark +4569918806 Finland Helsset +358942419041 Magyarország Budapest +3619980547 Ireland Dublin +35316526556 Luxembourg +35220880274 Norge Oslo +4721031366 Sverige Stockholm +46852503438 Schweiz Züri +41435006251 US New York +17185132983 |