Bifluranol

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Engineered Monoclonal Antibodies[edit source]

Diagram of engineered monoclonal antibodies

Engineered monoclonal antibodies are a class of biological therapies that are designed to target specific antigens on the surface of cells. These antibodies are produced using recombinant DNA technologies and are used in the treatment of various diseases, including cancer, autoimmune disorders, and infectious diseases.

Structure and Function[edit source]

Monoclonal antibodies are composed of two identical heavy chains and two identical light chains, forming a Y-shaped molecule. The tips of the "Y" contain the antigen-binding sites, which are highly specific to the target antigen. This specificity allows monoclonal antibodies to bind to their target with high affinity, blocking or modulating the function of the antigen.

Types of Engineered Monoclonal Antibodies[edit source]

There are several types of engineered monoclonal antibodies, each designed for specific therapeutic purposes:

  • Chimeric antibodies: These antibodies are composed of murine (mouse) variable regions and human constant regions. They are less immunogenic than fully murine antibodies.
  • Humanized antibodies: These antibodies are mostly human, with only the antigen-binding sites derived from murine sources. This reduces the risk of immune reactions.
  • Fully human antibodies: These are entirely human in origin, produced using transgenic mice or phage display technologies.
  • Bispecific antibodies: These antibodies are engineered to bind two different antigens simultaneously, offering unique therapeutic mechanisms.

Applications in Medicine[edit source]

Engineered monoclonal antibodies have revolutionized the treatment of many diseases:

  • Cancer therapy: Monoclonal antibodies can target specific tumor antigens, leading to direct tumor cell killing or recruitment of immune cells to attack the tumor.
  • Autoimmune diseases: By targeting specific components of the immune system, monoclonal antibodies can reduce inflammation and tissue damage in diseases such as rheumatoid arthritis and multiple sclerosis.
  • Infectious diseases: Monoclonal antibodies can neutralize pathogens or their toxins, providing passive immunity or enhancing the host's immune response.

Production[edit source]

The production of engineered monoclonal antibodies involves several steps:

1. Antigen identification: The target antigen is identified and characterized. 2. Hybridoma technology: B cells from immunized animals are fused with myeloma cells to create hybridomas that produce the desired antibody. 3. Recombinant DNA technology: Genes encoding the antibody are cloned and expressed in suitable host cells, such as Chinese hamster ovary cells. 4. Purification and formulation: The antibodies are purified and formulated for clinical use.

Challenges and Future Directions[edit source]

While engineered monoclonal antibodies have shown great promise, there are challenges such as high production costs, potential for immune reactions, and the development of resistance. Ongoing research aims to improve antibody design, reduce immunogenicity, and enhance therapeutic efficacy.

Related Pages[edit source]

Bifluranol (INN , BAN

brand name Prostarex; former developmental code name BX-341) is a synthetic nonsteroidal estrogen of the stilbestrol group related to diethylstilbestrol that has been used as an antiandrogen in the United Kingdom in the treatment of benign prostatic hyperplasia.[1][2][3][4][5][6] It is a polyfluorinated biphenyl that is related to polybrominated and polychlorinated biphenyls and diethylstilbestrol.[4][7][8] The drug is described as a weak estrogen, and possesses about one-eighth the potency of diethylstilbestrol.[3][7][9]

In spite of the fact that it is widely referred to as an antiandrogen in the literature, bifluranol is actually a pure estrogen and does not significantly bind to the androgen receptor or directly antagonize the action of androgens.[3] It exerts functional antiandrogen effects by binding to and activating the estrogen receptor in the pituitary gland, consequently suppressing the secretion of luteinizing hormone (and hence acting as an antigonadotropin) and thereby reducing gonadal androgen production and systemic androgen levels.[3] Bifluranol has also been found to act as a 17α-hydroxylase/17,20 lyase inhibitor, though with less potency than ketoconazole, and this action may contribute to its efficacy in benign prostatic hyperplasia by further helping to lower androgen levels.[10][11][12]

Related drugs include pentafluranol (BX-430) and terfluranol (BX-428), which are also estrogens.[13]

See also[edit | edit source]

References[edit | edit source]

  1. ↑ {{{last}}}, J. Elks, The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. online version, Springer, ISBN 978-1-4757-2085-3, Pages: 152,
  2. ↑ , Index Nominum 2000: International Drug Directory. online version, Taylor & Francis, ISBN 978-3-88763-075-1, Pages: 124–,
  3. ↑ 3.0 3.1 3.2 3.3 , Anti-prostatic activity of bifluranol, a fluorinated bibenzyl., British Journal of Pharmacology, 1980, Vol. 71(Issue: 1), pp. 11–16, DOI: 10.1111/j.1476-5381.1980.tb10903.x, PMID: 6258683, PMC: 2044395,
  4. ↑ 4.0 4.1 , Bifluranol, a novel fluorinated bibenzyl anti-androgen, its chemistry and disposition in different animal species, Journal of Pharmacy and Pharmacology, 1981, Vol. 33(Issue: 1), pp. 297–301, DOI: 10.1111/j.2042-7158.1981.tb13784.x, PMID: 6116777,
  5. ↑ , Bifluranol in the treatment of benign prostatic hyperplasia (BPH), The Prostate, 1985, Vol. 7(Issue: 4), pp. 357–361, DOI: 10.1002/pros.2990070403,
  6. ↑ , Response of the Benign Hypertrophied Prostate to Treatment with an LHRH Analogue, British Journal of Urology, 1988, Vol. 62(Issue: 2), pp. 163–165, DOI: 10.1111/j.1464-410X.1988.tb04299.x, PMID: 2457404,
  7. ↑ 7.0 7.1 , 3rd World Congress of Animal Feeding. online version, Industrias Gráficas España, 1978, ISBN 978-84-7391-022-4,
  8. ↑ , Annual Reports in Medicinal Chemistry. online version, Academic Press, ISBN 978-0-08-058365-5, Pages: 182–,
  9. ↑ {{{last}}}, M. K. Agarwal, Receptor mediated antisteroid action. online version, De Gruyter, 1987, ISBN 978-0-89925-374-9,
  10. ↑ , Inhibition of 17α-hydroxylase/C17-C20 lyase by bifluranol and its analogues, Journal of Steroid Biochemistry, 1989, Vol. 33(Issue: 6), pp. 1191–1195, DOI: 10.1016/0022-4731(89)90429-9, PMID: 2559252,
  11. ↑ , Inhibitors of enzymes of androgen biosynthesis: cytochrome P45017α and 5α-steroid reductase, Natural Product Reports, 1998, Vol. 15(Issue: 5), pp. 495, DOI: 10.1039/a815495y,
  12. ↑ , Biochemistry and pharmacokinetics of potent non-steroidal cytochrome P45017α inhibitors, The Journal of Steroid Biochemistry and Molecular Biology, 1997, Vol. 60(Issue: 5-6), pp. 347–351, DOI: 10.1016/S0960-0760(96)00225-7,
  13. ↑ {{{last}}}, Polska Akademia Nauk. Komitet Badania Polonii, II Kongres Uczonych Polskiego Pochodzenia: zbiór materiałów. online version, Zakład Narodowy im. Ossolińskich, 1984, ISBN 978-83-04-01670-5,





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