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Статті в журналах з теми "FK-506 (Drug)":

1

Shaw, L. M., and K. L. Brayman. "FK-506 therapeutic drug monitoring." Clinical Chemistry 40, no. 12 (December 1, 1994): 2207–8. http://dx.doi.org/10.1093/clinchem/40.12.2207.

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2

Winkler, M., B. Ringe, J. Baumann, M. Loss, K. Wonigeit, and R. Pichlmayr. "Plasma vs whole blood for therapeutic drug monitoring of patients receiving FK 506 for immunosuppression." Clinical Chemistry 40, no. 12 (December 1, 1994): 2247–53. http://dx.doi.org/10.1093/clinchem/40.12.2247.

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Abstract By retrospective analysis of 13,000 blood samples obtained from 248 patients receiving FK 506 therapy, we compared the suitability of plasma with that of whole blood as the matrix for therapeutic drug monitoring of FK 506. The plasma concentrations did not correlate with the concentrations in whole blood (r = 0.56). In contrast to plasma samples (analyzed by enzyme immunoassay), FK 506 was detectable in all whole-blood samples (analyzed by enzyme immunoassay/microparticle enzyme immunoassay). The inter- and intraindividual variations of FK 506 measurements were greater in plasma than in whole blood. Moreover, plasma concentrations correlated only poorly with clinical events. There was a tendency to greater plasma concentrations being measured during episodes of toxicity, but no clear difference was evident between stable course and rejection. In whole-blood specimens, a correlation between reduced or increased FK 506 concentrations and rejection or toxicity, respectively, was observed. The discriminatory power of whole-blood values was greater for the differentiation between toxicity and stable course than between rejection and stable course. We therefore recommend whole blood rather than plasma as the matrix for therapeutic monitoring of FK 506 concentrations.
3

Dumont, F. J., M. J. Staruch, S. L. Koprak, J. J. Siekierka, C. S. Lin, R. Harrison, T. Sewell, V. M. Kindt, T. R. Beattie, and M. Wyvratt. "The immunosuppressive and toxic effects of FK-506 are mechanistically related: pharmacology of a novel antagonist of FK-506 and rapamycin." Journal of Experimental Medicine 176, no. 3 (September 1, 1992): 751–60. http://dx.doi.org/10.1084/jem.176.3.751.

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FK-506 inhibits Ca(2+)-dependent transcription of lymphokine genes in T cells, and thereby acts as a powerful immunosuppressant. However, its potential therapeutic applications may be seriously limited by several side effects, including nephrotoxicity and neurotoxicity. At present, it is unclear whether these immunosuppressive and toxic effects result from interference with related biochemical processes. FK-506 is known to interact with FK-binding protein-12 (FKBP-12), an abundant cytosolic protein with cis-trans peptidyl-prolyl isomerase activity (PPIase) activity. Because rapamycin (RAP) similarly binds to FKBP-12, although it acts in a manner different from FK-506, by inhibiting T cell responses to lymphokines, such an interaction with FKBP-12 is not sufficient to mediate immunosuppression. Recently, it was found that the complex of FKBP-12 with FK-506, but not with RAP, inhibits the phosphatase activity of calcineurin. Here, we used L-685,818, the C18-hydroxy, C21-ethyl derivative of FK-506, to explore further the role of FKBP-12 in the immunosuppressive and toxic actions of FK-506. Although L-685,818 bound with high affinity to FKBP-12 and inhibited its PPIase activity, it did not suppress T cell activation, and, when complexed with FKBP-12, did not affect calcineurin phosphatase activity. However, L-685,818 was a potent antagonist of the immunosuppressive activity of both FK-506 and RAP. Moreover, L-685,818 did not induce any toxicity in dogs and rats or in a mouse model of acute FK-506 nephrotoxicity, but it blocked the effect of FK-506 in this model. Therefore, FK-506 toxicity involves the disruption of biochemical mechanisms related to those implicated in T cell activation. Like immunosuppression, this toxicity is not due to the inhibition of the PPIase activity of FKBP-12, but may be linked to the inhibition of the phosphatase activity of calcineurin by the drug FKBP-12 complex.
4

Rokaw, M. D., M. E. West, P. M. Palevsky, and J. P. Johnson. "FK-506 and rapamycin but not cyclosporin inhibit aldosterone-stimulated sodium transport in A6 cells." American Journal of Physiology-Cell Physiology 271, no. 1 (July 1, 1996): C194—C202. http://dx.doi.org/10.1152/ajpcell.1996.271.1.c194.

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The immunosuppressants cyclosporin A (CyA), FK-506, and rapamycin (RAP) have multiple actions on target cells that appear to be mediated by interaction of drug-binding protein complexes. Both FK-506 and CyA, but not RAP, inhibit the Ca2(+)-dependent phosphatase, calcineurin, and in so doing have been found to inhibit Na(+)-K(+)-ATPase activity in various nephron segments. Of interest, FK-506 and RAP, but not CyA, are bound by the steroid receptor-associated FK-506-binding heat shock protein of 56 kDa, HSP56. To determine the physiological effect of this interaction on a steroid-mediated phenomenon, the effect of these agents on steroid-mediated Na+ transport in A6 cells was investigated. Aldosterone stimulation of Na+ transport and Na(+)-K(+)-ATPase activity are significantly inhibited by prolonged incubation with FK-506 and RAP. Although CyA inhibits basal Na(+)-K(+)-ATPase activity, it has no effect on aldosterone-induced Na+ transport or the aldosterone-induced increase in Na(+)-K(+)-ATPase activity. FK-506 inhibits the aldosterone-induced synthesis of G alpha i-3 protein but has no effect on glucocorticoid receptor number as quantified by Western blotting. The results suggest that FK-506 and RAP inhibit steroid-mediated Na+ transport at some pretranslational site. The common interaction of these agents with the steroid receptor-associated HSP56 might account for these findings.
5

Di Padova, F. E. "Pharmacology of CsA and FK-506." Perspectives in Drug Discovery and Design 2, no. 1 (August 1994): 49–56. http://dx.doi.org/10.1007/bf02171736.

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6

Goulet, Mark T., Kathleen M. Rupprecht, Peter J. Sinclair, Matthew J. Wyvratt, and William H. Parsons. "The medicinal chemistry of FK-506." Perspectives in Drug Discovery and Design 2, no. 1 (August 1994): 145–62. http://dx.doi.org/10.1007/bf02171741.

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7

Petros, Andrew M., Gerd Gemmecker, Placido Neri, Edward T. Olejniczak, David Nettesheim, Robert X. Xu, Earl G. Gubbins, Harriet Smith, and Stephen W. Fesik. "NMR studies of an FK-506 analog, [U-carbon-13]ascomycin, bound to FK-506-binding protein." Journal of Medicinal Chemistry 35, no. 13 (June 1992): 2467–73. http://dx.doi.org/10.1021/jm00091a015.

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8

Kay, John E., Senam E. A. Doe, and C. Robin Benzie. "The mechanism of action of the immunosuppressive drug FK-506." Cellular Immunology 124, no. 1 (November 1989): 175–81. http://dx.doi.org/10.1016/0008-8749(89)90121-4.

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9

O'connor, Stephen P., Robert L. Ellsworth, Mary Nallin Omstead, Rosalind G. Jenkins, and Louis Kaplan. "The preparation of 14C-labeled FK-506." Journal of Labelled Compounds and Radiopharmaceuticals 31, no. 2 (February 1992): 103–8. http://dx.doi.org/10.1002/jlcr.2580310205.

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10

Jusko, William J. "Analysis of Tacrolimus (FK 506) in Relation to Therapeutic Drug Monitoring." Therapeutic Drug Monitoring 17, no. 6 (December 1995): 596–601. http://dx.doi.org/10.1097/00007691-199512000-00009.

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Дисертації з теми "FK-506 (Drug)":

1

Karlsson, Håkan. "Influence of FK506 on certain aspects of lymphocyte activation and lymphocyte-endothelial cell interactions in vitro." Lund : Dept. of Medical Microbiology, Section of Clinical Immunology, Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/39799195.html.

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2

Whitaker, Audie D. "The role of interferon-gamma in cyclosporine A or FK-506 treated L. major infected mice." Virtual Press, 1999. http://liblink.bsu.edu/uhtbin/catkey/1138295.

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Certain strains of mice, e.g. C57BL/6, are highly resistant to serious infections with the protozoan pathogen, Leishmania major, whereas other strains, e.g. BALB/c, are not. It has beenproposed that interferon gamma (IFN-y) is one of the most critical lymphokines produced in a protective response to these intracellular pathogens. IFN-y has been classified as a Thi lymphokine produced by the Thl subset of T lymphocytes which not only activates macrophages to kill the protozoa but also helps regulates the immune system overall to form a lasting immunity to the microorganism (4,19). Mice susceptible to L. major arethought to produce inadequate amounts of IFN-y and instead produce an excessive amount of a Th2 lymphokine, IL-4, produced by Th2 T cells. (6) We have previously found that prophylactic treatment with cyclosporine A (CsA), a T cell specific immunosuppressant, reduces the susceptibility of the BALB/c to L. major by either preventing disease entirely or delaying itsdevelopment significantly (19). In this murine model, it may be that CsA causes a switch from the production of the less protective Th2 lymphokines to the more protective Thl lymphokines. In order to test this hypothesis we examined the IFN-y produced by lymph node and spleen cells over time after infection in three groups of mice: C57BL/6, BALB/c and cyclosporine- protected BALB/c. Interestingly, cells taken from all three groups of mice were able to secrete IFN-y in vitro in response to co-culture with Leishmania, antigens. The pattern of secretion over time, however, varied and may indicate a significant difference in the animals' response to the pathogen. In addition to this work, we also examined the ability of another immunosuppressant, FK506, which is very similar in action to but much less toxic than CsA, to induce enhanced resistence to L. major. FK506 also appears to be effective in reversing the susceptibility of the BALB/c mice towards this pathogen with much less apparent toxicity.
Department of Biology
3

Potter, Shannon M. "The role of cyclosporin A, leptin, and FK-506 in Leishmania major infections in mice." Muncie, Ind. : Ball State University, 2009. http://cardinalscholar.bsu.edu/467.

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4

Jones, Terence Edward. "Economically beneficial drug interactions with cyclosporin and tacroliumus : clinical studies in recipients of kidney and liver transplants." Title page, contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phj79.pdf.

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Bibliography: leaves 234-257. Three separate clinical studies in organ transplant recipients are presented. The aims are to examine fundamental questions regarding the clinically and economically important pharmokinetic interaction between diltiazem and cyclosporin, an interaction widely utilised in organ transplantation. The data contained should assist the development of soundly based policies that will ensure a benefit exists before a sparing agent is coprescribed, and that the lowest effective dose of sparing agent is used.
5

Soubhia, Rosa Maria Cordeiro. "Avaliação dos efeitos nefrotóxicos da associação do tacrolimus (FK 506) e antiinflamatórios não-hormonais em ratos." Faculdade de Medicina de São José do Rio Preto, 2005. http://bdtd.famerp.br/handle/tede/166.

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Made available in DSpace on 2016-01-26T12:51:42Z (GMT). No. of bitstreams: 1 rosasoubhia_tese.pdf: 792706 bytes, checksum: bba71696e22270729d09c3130cc047eb (MD5) Previous issue date: 2005-05-25
Introduction: Tacrolimus (FK 506) is a potent immunosuppressive drug that may cause nephrotoxicity decreasing the renal blood flow (RBF) and glomerular filtration rate (GFR). Conventional non-steroidal anti-inflammatory drugs (NSAIDs) may cause nephrotoxicity, interfering with renal hemodynamics and fluid and eletrolyte homeostasis. Recently, new selective COX-2 inhibitors have been developed producing less side effects (gastric, cardiac and renal) related to COX-1 inhibition. The increasing use of FK 506 and the intensive use of NSAIDs with analgesic or ani-inflammatory purposes, increases the possibility of a drug combination, potentiating the nephrotoxic risk of the two drugs. Objective : Compare the renal function of rats receiving combination therapy with FK and a non-selective COX inhibitor, sodium diclofenac (SD) with those receiving FK and a selective COX-2 inhibitor, rofecoxib (RO). Material and Methods : Male Munich-Wistar rats receiving a low sodium diet (0.06%) for 7 days and gavage treatment for 7 days with FK (2 mg/kg/day), SD (10 mg/kg/day), RO (3 mg/kg/day), FK+SD, FK+RO and vehicle (control) were used. Glomerular filtration rate (GFR, inulin clearance, ml/min/100g); renal blood flow (RBF, Doppler ultrasound, ml/min); mean blood pressure (MBP, intracarotid probe, mmHg); renal vascular resistence ( RVR, mmHg/ml/min); hematocrit (Htc); urinary volume ( UV, μl/min); solute clearance; renal histology; animal weight (g) and FK serum concentration (SCFK, ng/ml) were assessed. Results are presented as a mean±standart deviation and compared by ANOVA followed by Student-Neuman-Keuls test. Results : The GRF of the SD group was 0.98±0.03, RO 1.06±0.04 and FK 0.99±0.06 similar to control values (1.10±0.05). GRF values decreased in the FK+RO (0.86±0.06;p<0.05 vs RO and Control) and FK+SD (0.63±0.06;p<0.001 vs control, FK and SD groups and p<0.01 vs FK+RO) groups. RBF, MBP, RVR and Htc values were similar in all groups. Diuresis was lower in the groups with drug combination, but there was a statistically significant difference only between FK+SD and RO groups (8.38±0.46 vs 12.99±1.22;p<0.05). There were no significant histological chan ges in the treatment groups. The FK+SD group showed statistically significant weigth changes (-18±5) when compared to the Control and RO groups (6±2 and 5±2, respectively; p<0.001) and to the SD an FK+RO groups (0.2±4 and 1±2, respectively; p<0.01). SCFK was significantly decreased (p<0.05) for FK+SD and FK+RO (1.7±0.3 and 1.8±0.4) groups when compared to the FK group (3.2±0.4. Conclusions: The combination of FK and a non-selective COX inhibitor significantly decreased GFR regardless of a RBF decrease or RVR increase, and is probably a result of Kf decrease. The trend to antidiuresis was similar for the combination of FK with both classes of NSAIDs. FK combined to a non-selective COX inhibitor caused a mild systemic toxicity when compared with the COX-2 selective inhibitor. Serum FK concentrations were significantly lower in NSAIDs treated animals.
Introdução: O tacrolimus (FK 506) é uma potente droga imunossupressora, pode causar nefrotoxicidade aguda com diminuição do fluxo sanguíneo renal (FSR) e ritmo de filtração glomerular (RFG). Os antiinflamatórios não-hormonais (AINHs) convencionais podem causar nefrotoxicidade, interferindo na hemodinâmica renal e na homeostase de fluidos e eletrólitos. Recentemente surgiram novas drogas do grupo coxib que são inibidores seletivos da COX-2, e portanto teriam menos efeitos colaterais relacionados à inibição da COX-1 (gástricos, cardíacos e renais). O crescente uso do FK 506 e o intenso uso de AINHs com finalidade analgésica e ou antiinflamatória aumenta a possibilidade de utilização em conjunto, potencializando o risco de nefrotoxicidade das duas drogas. Objetivo: Comparar a função renal de ratos sob os efeitos do uso simultâneo do FK e de um inibidor não-seletivo da COX, o diclofenaco sódico (DS) e do FK e de um inibidor seletivo da COX-2, o rofecoxib (RO). Materiais e Método: Utilizaram-se ratos Munich-Wistar machos em dieta hipossódica (0,06%) por 7 dias e tratamento por gavagem por 7 dias com FK (2 mg/kg/dia), DS (l0mg/kg/dia), RO (3mg/kg/dia), FK+DS, FK+RO e veículo (Contr). Aferidos ritmo de filtração glomerular (RFG, depuração de inulina, ml/min/l00g); o fluxo sanguíneo renal (FSR, ultrasom Doppler, ml/min); a pressão arterial média (PAM, probe intracarotídeo, mmHg); a resistência vascular renal (RVR, mmHg/ml/min); hematócríto (Ht); o volume urinário (VU, pl/min); a depuração de solutos; a histologia renal; o peso dos animais (g) e a concentração sanguínea de FK CSFK, ng/ml). Os resultados são apresentados com médiaserro padrão da média e comparados por ANOVA seguido do teste Student-Neuman-Keuls. Resultados: O RFG do grupo DS foi 0,980,03, do RO foi 1,060,04 e do FK 0,990,06 similares ao controle (1,100,05). Houve queda do RFG nos grupos FK+RO (0,860,06;p<0,Os vs RO e Contr) e FK+DS (0,630,06;p<0,001 vs Contr,DS, RO e FK; p<0,01 vs FK+RO) Nota de Resumo O FSR, a PAM, a RVR e o Ht foram semelhantes em todos os grupos. A diurese foi menor nos grupos com associação de drogas, mas houve diferença estatisticamente significante apenas entre os grupos FK+DS e RO (8,380,46 vs l299l,22;p<0,05). Não ocorreram modificações histológicas significativas nos grupos estudados. O grupo FK+DS apresentou variação de peso (-185) estatisticamente significante em relação aos grupos Contr 62 e RO 52 (p<0,001) e DS 0,24 e FK+RO -12 (p<0,01). A CSFK diminuiu significativamente (p<0,05) para os grupos FK+DS e FK+RO (1,70,3 e 1,80,4) em relação ao grupo FK (3,20,4). Conclusões: A associação do FK com um inibidor não-seletivo da COX causou diminuição mais acentuada do RFG independentemente da diminuição do FSR ou aumento da RVR, sendo provavelmente decorrente da diminuição do Kf. A tendência à antidiurese foi similar para a associação do FK com as duas classes de AINHs. O FK associado com um inibidor não-seletivo da COX causou discreta toxicidade sistêmica quando comparado com inibidor seletivo da COX-2. Nos animais tratados com AINHs, as concentrações sanguíneas do FK foram significativamente menores.
6

Toske, Steven Gerald. "Part I : synthesis of azetidin-2-ones from pyrazolidin-3-ones ; Part II : synthesis of a subunit of the immunosuppressant FK-506." Thesis, 1993. http://hdl.handle.net/1957/35676.

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7

Sinswat, Prapasri 1972. "Enhancing the delivery of poorly water soluble drugs using particle engineering technologies." 2006. http://hdl.handle.net/2152/13124.

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8

Overhoff, Kirk Alan. "Improved oral bioavailability of poorly water soluble drugs using rapid freezing processes." 2006. http://hdl.handle.net/2152/13125.

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A growing number of therapeutic compounds currently being developed by pharmaceutical companies are poorly water soluble leading to limited and/or erratic bioavailability. The rate limiting step for absorption of these compounds is dependent on the dissolution and apparent solubility. Nanoparticle formation has been exploited as a method to improve the bioavailability of these poorly water soluble active pharmaceutical ingredients (API) by increasing the dissolution rates and apparent solubilities. The influence of hydrophilic stabilizers in powder compositions prepared by the spray freezing into liquid (SFL) process using either an emulsion feed dispersion or organic co-solvent feed solutions on enhancing the wetting and dissolution properties of nanostructured aggregates containing itraconazole (ITZ). Subsequently, an in vivo pharmacokinetic study was conducted comparing the SFL processed powder to commercial Sporanox®. An ultra-rapid freezing (URF) technology has been developed to produce high surface area powders composed of solid solutions of an active pharmaceutical ingredient (API) and a polymer stabilizer. Rapid freezing technologies are known to enhance the physico-chemical properties of APIs and thus increase bioavailability. However, the effect of the different freezing geometries and rates in the URF process are unknown. Therefore, this study investigated how solvent properties and thin film geometry of the droplet affect the freezing rate and thus the physico-chemical properties of micronized danazol powders. Amorphous nanoparticles containing tacrolimus (TAC) in a solid dispersion were prepared using the Ultra-rapid Freezing (URF) process. The objective of this study was to assess the effects of combinations of polymeric stabilizers on the maximum degree and extent of supersaturation of TAC. An attempt to establish if an in vitro-in vivo correlation exists between supersaturation and improved pharmacokinetic parameters for orally dosed TAC was performed. Enteric solid dispersions could overcome limitations of premature precipitation of supersaturated solutions by 1.) delaying dissolution until the compound enters the intestines where absorption is favored and 2.) increasing the apparent solubility at higher pH to increase the driving force for absorption. The objective of the study is to investigate the influence of composition parameters including drug:polymer ratio and polymer type, and particle structure of enteric solid dispersions on the release of ITZ.
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Книги з теми "FK-506 (Drug)":

1

Steinmuller, Donald R. FK506 and organ transplantation. Austin: R.G. Landes, 1994.

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2

Raptis, Dimitrios, and Manousos-Georgios Pramateftakis. Tacrolimus: Effectiveness, Safety and Drug Interactions. Nova Science Publishers, Incorporated, 2013.

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3

Tacrolimus in organ transplantation: Prevention and treatment of allograft rejections. Lengerich: Pabst Science Publishers, 1998.

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4

Toske, Steven Gerald. Part I: Synthesis of azetidin-2-ones from pyrazolidin-3-ones ; Part II : synthesis of a subunit of the immunosuppressant FK-506. 1993.

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5

Thomas, Ruzicka, and Reitamo Sakari, eds. Tacrolimus ointment: A topical immunomodulator for atopic dermatitis. Berlin: Springer, 2004.

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6

(Editor), T. Ruzicka, and S. Reitamo (Editor), eds. Tacrolimus. Springer, 2003.

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7

Tacrolimus ointment: A topical immunomodulator for atopic dermatitis. Berlin: Springer, 2003.

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Частини книг з теми "FK-506 (Drug)":

1

Rossaro, L., S. R. Dowd, V. Simplaceanu, R. Naccarato, D. H. Van Thiel, and C. Ho. "Effect of FK 506 and Cyclosporins on Model Membranes Studied by Nuclear Magnetic Resonance Spectroscopy." In Drugs and the Liver: High Risk Patients and Transplantation, 177–84. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1994-8_29.

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2

"Tacrolimus (FK-506)." In Drug Therapy in Dermatology, 172–81. CRC Press, 2000. http://dx.doi.org/10.1201/b14006-12.

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3

KOCIENSKI, PHILIP, MICHAEL STOCKS, and DAVID K. DONALD. "Recent Progress in Research on the Immunosuppressant FK-506." In Chirality in Drug Design and Synthesis, 131–65. Elsevier, 1990. http://dx.doi.org/10.1016/b978-0-12-136670-4.50014-x.

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