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Journal articles on the topic 'Cyclosporin'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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1

Charuk, J. H., P. Y. Wong, and R. A. Reithmeier. "Differential interaction of human renal P-glycoprotein with various metabolites and analogues of cyclosporin A." American Journal of Physiology-Renal Physiology 269, no. 1 (July 1, 1995): F31—F39. http://dx.doi.org/10.1152/ajprenal.1995.269.1.f31.

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Interactions of P-glycoprotein with several analogues and metabolites of cyclosporin A were studied to gain a better understanding of this immunosuppressant's mechanism of excretion and nephrotoxicity. Incorporation of [3H]azidopine into human renal P-glycoprotein in the presence of various concentrations of different cyclosporins was quantitated. Competitive [3H]azidopine photolabeling and 3H drug transport assays of CHRC5 multidrug-resistant cells were also conducted to evaluate effects of cyclosporins on P-glycoprotein function. Cyclosporins A [half-maximal inhibition constant (K0.5) = 20 nM] and G (K0.5 = 40 nM) blocked [3H]azidopine photolabeling of renal P-glycoprotein at very low concentrations, whereas higher concentrations of cyclosporin C (K0.5 = 500 nM) and metabolites 1, 17, and 21 (K0.5 = 200 nM) were required to inhibit photolabeling. Metabolites H and 8 were ineffective in inhibition of [3H]azidopine photolabeling of human renal P-glycoprotein. Similarly, cyclosporins A, C, and G were the best inhibitors of [3H]azidopine photolabeling of P-glycoprotein in multidrug-resistant C5 cells; the various metabolites were less effective. Cyclosporins A, C, and G also enhanced cellular accumulation of [3H]cyclosporin A and several other 3H-labeled compounds known to be transported by P-glycoprotein in multidrug-resistant C5 cells. Differential affinities of cyclosporin A metabolites for P-glycoprotein suggest considerable drug-binding site specificity. Our current hypothesis is that cyclosporin A may be more nephrotoxic than its metabolites by virtue of its superior ability to bind to and competitively inhibit urinary excretion of an endogenous P-glycoprotein substrate. Our findings provide the basis for future design and testing of new cyclosporin derivatives that have immunosuppressive activity yet may be less nephrotoxic because of their poor interaction with renal P-glycoprotein.

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2

Hušák, Michal, Bohumil Kratochvíl, Martin Buchta, Ladislav Cvak, and Alexandr Jegorov. "Crystal Structure of Cyclosporin E." Collection of Czechoslovak Chemical Communications 63, no. 1 (1998): 115–20. http://dx.doi.org/10.1135/cccc19980115.

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The structure of cyclosporin E was determined by X-ray diffraction methods and compared with the structure of related cyclosporins. In contrast to cyclosporin A, which crystallizes from acetone as tetragonal dihydrate, cyclosporin E acetone solvate monohydrate (C61H109N11O12·C3H6O·H2O) crystallizes under the same conditions in the monoclinic space group P21 with a = 15.698(2) Å, b = 21.333(3) Å, c = 13.224(2) Å, β = 103.74(1)°, Z = 2, and V = 4 302(1) Å3.

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3

Traber, R., H. Kobel, H. R. Loosli, H. Senn, B. Rosenwirth, and A. Lawen. "[Melle4]Cyclosporin, a Novel Natural Cyclosporin with anti-HIV Activity: Structural Elucidation, Biosynthesis and Biological Properties." Antiviral Chemistry and Chemotherapy 5, no. 5 (October 1994): 331–39. http://dx.doi.org/10.1177/095632029400500507.

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From fermentations of Tolypocladium niveum supplemented with D-threonine, a novel natural cyclosporin, [Melle4]cyclosporin, was isolated. Its structural elucidation is based on amino acid analysis and spectroscopic data; the amino acid sequence was deduced from two-dimensional NMR investigations applied to the iso-derivative of [Melle4]cyclosporin which, in contrast to the natural product, is present as one homogenous conformation in solution. We show that one of the four N-methyl-L-leucine units of cyclosporin A, namely that in position 4, is replaced by N-methyl-L-isoleucine. The putative mechanism by which D-threonine induces in vivo biosynthesis of [Melle4]cyclosporin is discussed. In vitro biosynthesis of [Melle4]cyclosporin was achieved using the previously described enzymatic system [Lawen and Traber (1993) J Biol Chem268: 20452–20465], thereby demonstrating the high affinity of cyclosporin synthetase for isoleucine in position 4. In a long series of cyclosporins obtained by in vitro and in vivo biosynthesis, [Melle4]cyclosporin represents the first example that is devoid of immunosuppressive efficacy while retaining strong binding to cyclophilin. It exerts potent in vitro anti-HIV-1 activity.

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4

Lawen, A., R. Traber, R. Reuille, and M. Ponelle. "In vitro biosynthesis of ring-extended cyclosporins." Biochemical Journal 300, no. 2 (June 1, 1994): 395–99. http://dx.doi.org/10.1042/bj3000395.

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Cyclosporin synthetase, a multifunctional polypeptide, catalyses the biosynthesis of the set of natural cyclosporins. We report that this enzyme is also capable of introducing a beta-alanine into position 7 or 8 of the ring instead of the alpha-alanines present at these positions in cyclosporin A. This leads to 34-membered rings in contrast to the 33-membered ring of the cyclo-undecapeptide cyclosporin A. Both [beta Ala7]CyA and [beta Ala8]CyA show immunosuppressive activity. The cyclosporin synthetase-related enzyme peptolide SDZ 214-103 synthetase, on the other hand, does not incorporate either beta-alanine into position 7 or beta-hydroxy acids into position 8, confirming the previously described higher substrate specificity of this enzyme compared with cyclosporin synthetase [Lawen and Traber (1993) J. Biol. Chem. 268, 20452-20465].

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5

Schramm, U., G. Fricker, R. Wenger, and D. S. Miller. "P-glycoprotein-mediated secretion of a fluorescent cyclosporin analogue by teleost renal proximal tubules." American Journal of Physiology-Renal Physiology 268, no. 1 (January 1, 1995): F46—F52. http://dx.doi.org/10.1152/ajprenal.1995.268.1.f46.

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The transport of a fluorescent cyclosporin analogue was measured in killifish (Fundulus heteroclitus) proximal tubules by means of epifluorescence microscopy and digital image analysis. Renal cells rapidly accumulated the cyclosporin analogue from the medium and attained steady state within 60 min; luminal fluorescence increased over the first 60-90 min. At steady state, luminal fluorescence intensity was two to three times higher than cellular. Cellular fluorescence intensity was a linear function of medium substrate concentration and was not affected by any treatment used. In contrast, luminal fluorescence exhibited a saturable component as the medium concentration of the cyclosporin was increased. Secretion into the lumen was blocked by metabolic inhibitors, vanadate, other cyclosporins, such as cyclosporin A and cyclosporin G, and substrates for P-glycoprotein (verapamil, vinblastine, and quinine) but not by substrates for the renal organic anion or organic cation transport systems, such as p-aminohippurate or tetraethylammonium. The data are consistent with the fluorescent cyclosporin analogue entering proximal tubule cells by simple diffusion and then being pumped into the tubular lumen by P-glycoprotein.

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6

Langman, L., D. LeGatt, and R. Yatscoff. "Cross-reactivities of cyclosporin G (NVa2 cyclosporin) and metabolites in cyclosporine A immunoassays." Clinical Biochemistry 26, no. 2 (April 1993): 122. http://dx.doi.org/10.1016/0009-9120(93)90040-d.

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7

Kratochvíl, Bohumil, Alexandr Jegorov, Svetlana Pakhomova, Michal Hušák, Petr Bulej, Ladislav Cvak, Petr Sedmera, and Vladimír Havlíček. "Crystal Structures of Cyclosporin Derivatives: O-Acetyl-(4R)-4-(E-2-butyl)-4,N-dimethyl-L-threonyl-cyclosporin A and O-Acetyl-(4R)-4-[E-2-(4-bromobutyl)]-4,N-dimethyl-L-threonyl-cyclosporin A." Collection of Czechoslovak Chemical Communications 64, no. 1 (1999): 89–98. http://dx.doi.org/10.1135/cccc19990089.

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The structures of O-acetyl-(4R)-4-(E-2-butyl)-4,N-dimethyl-L-threonyl-cyclosporin A (1) and O-acetyl-(4R)-4-[E-2-(4-bromobutyl)]-4,N-dimethyl-L-threonyl-cyclosporin A (2) were determined by X-ray diffraction methods and compared with the structure of related cyclosporins. In contrast to expectation, neither the acetylation nor the subsequent bromination of 1 affects the conformation and packing of cyclosporins in the solid state. Both compounds are isomorphous and crystallize in the orthorhombic space group P212121 with a = 12.936(2) Å, b = 15.590(2) Å, c = 36.280(3) Å, and a = 12.916(3) Å, b = 15.675(4) Å, c = 36.715(7) Å, for 1 and 2, respectively.

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8

Elbakidze, G. M., A. G. Medentsev, and A. G. Elbakidze. "INFLUENCE OF PRODIGIOZAN-DEPENDENT COMUTON ON THE RESISTANCE OF LIVER MITOCHONDRIA AGAINST DAMAGE BY PROTONOFOR." Annals of the Russian academy of medical sciences 69, no. 1-2 (August 20, 2015): 75–79. http://dx.doi.org/10.15690/vramn.v69.i1-2.946.

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An effector of tissue stress of hepatocytes, prodigiozan-dependent comuton (PDC), provokes deenergiezation of liver mitochondria, preloaded by Ca2+ ions. In this case a decrease of membrane potential (MP) and Ca2+ efflux by cyclosporine A sensitive mechanism of megapore is observed. If megapore is blocked by cyclosporin A, protonofor FCCP provoked decrease of MP and Ca2+ efflux by cyclosporin A-insensitive mechanism. It is shown that PDC increases resistance of mitochondria to mentioned protonofor action by inhibition of both these effects. An inhibitory action of PDC is realized by K+ and NADH-dependent mechanism. The effector of hepatocyte tissue stress, prodigiozan-dependent comuton (PDC), evokes deenergizing liver mitochondria preloaded with Ca2+, both membrane potential (MP) decrease and Ca2+ release in according to cyclosporine A- sensitive mechanism of megapore being observed. If megapore is blocked by cyclosporin A, protonophore FCCP reduces of MP and Ca2+ release in according to cyclosporin A-insensitive mechanism. PDC is shown to increase the resistance of mitochondria against protonophore action mentioned above by means of inhibition of both these effects. Inhibitory action of PDC is realized due to both K+ and NADH-dependent mechanism. protective effect takes place only in intact mitochondria of these cells providig (on condition that) its megapore mechanism is not activated. Moreover, the results obttained are evidence of PDC can function as protector due to intensification of energy generation in damaged.

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9

Kim, J. Y., S. H. Park, K. S. Cho, H. J. Kim, C. K. Lee, K. K. Park, S. H. Choi, and W. Y. Chung. "Mechanism of Azithromycin Treatment on Gingival Overgrowth." Journal of Dental Research 87, no. 11 (November 2008): 1075–79. http://dx.doi.org/10.1177/154405910808701110.

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Azithromycin is effective for the remission of cyclosporine A-induced gingival overgrowth (CIGO) in persons who have undergone renal transplant. To explain its mechanism in alleviating the clinical symptoms of these indivduals, we examined the effect of azithromycin on cell proliferation and collagen turnover modified by cyclosporin A in human gingival fibroblasts from healthy persons and from persons who had undergone renal transplant. Cyclosporin A-induced proliferation of renal transplant fibroblasts and normal fibroblasts was inhibited by azithromycin. Azithromycin elevated the reduced metalloproteinase (MMP)-1 and MMP-2 activities in cyclosporine A-treated renal transplant fibroblasts and normal fibroblasts. In cyclosporine A-treated renal transplant fibroblasts, azithromycin blocked the accumulation of total collagen in culture media and the increase in type I collagen mRNA level, but recovered the reduced MMP-2 mRNA level to the control. These results suggest that azithromycin may improve CIGO by blocking cyclosporine A-induced cell proliferation and collagen synthesis, and by activating MMP-2 in gingival fibroblasts of persons with cyclosporine A-induced gingival overgrowth.

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10

&NA;. "Cyclosporin see Minoxidil/cyclosporin." Reactions Weekly &NA;, no. 312 (August 1990): 6. http://dx.doi.org/10.2165/00128415-199003120-00024.

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11

&NA;. "Cyclosporin see Azathioprine/cyclosporin." Reactions Weekly &NA;, no. 331 (December 1990): 6. http://dx.doi.org/10.2165/00128415-199003310-00029.

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12

&NA;. "Cyclosporin see Aminoglycosides + cyclosporin." Reactions Weekly &NA;, no. 365 (August 1991): 6. http://dx.doi.org/10.2165/00128415-199103650-00021.

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13

Feliciani, Claudio, Anna Zampetti, Pietro Forleo, Luca Cerritelli, Paolo Amerio, Gianluca Proietto, Antonio Tulli, and Pierluigi Amerio. "Nail Psoriasis: Combined Therapy with Systemic Cyclosporin and Topical Calcipotriol." Journal of Cutaneous Medicine and Surgery 8, no. 2 (March 2004): 122–25. http://dx.doi.org/10.1177/120347540400800208.

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Background: Nail psoriasis is a common problem in psoriatic patients and often it is difficult to cure. Several treatments have been proposed in the last decade using new molecules like vitamin-D analog and/or immunosuppressive drugs both systemically and locally. Objective: Our goal was to evaluate a combination of cyclosporin and topical calcipotriol cream versus cyclosporin alone in a matched group of patients treated with cyclosporin alone. Method: Fifty-four patients affected by severe psoriasis and nail involvement were selected and matched for severity of nail involvement, sex, age, and cyclosporin dosage. Group A included 21 patients treated with cyclosporin alone (3.5 mg/kg/day) for three months. Group B included 33 patients treated with the same cyclosporin dosage plus, for the same time, topical application of calcipotriol cream twice a day. Evaluation for clinical improvement was the personal feeling of the patient after three months, while clinical appearance of the lesions was evaluated by the same dermatologist using digital pictures and who was blind as to the treatment of the patient. A score ranging from + to +++ was used in order to evaluate the improvement, and data were statistically evaluated with the Wilcoxon test. Results: Both cyclosporin alone and a combination of cyclosporin with topical calcipotriol twice a day were useful for treating nail psoriasis after three months of therapy although the combined therapy showed a better overall result in both mild and severe nail psoriasis. Improvement of the clinical appearance of the nail lesions was seen in about 79% of patients in group B ( p ≤ 0.0004) versus about 47% of patients in group A ( p ≤ 0.15). Conclusionsln patients with severe involvement of nail psoriasis we suggest the use of a combination of topical calcipotriol twice a day with systemic treatment such as cyclosporine.

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14

Feliciani, C., and A. Tulli. "Topical Cyclosporin in the Treatment of Dermatologic Diseases." International Journal of Immunopathology and Pharmacology 15, no. 2 (May 2002): 89–93. http://dx.doi.org/10.1177/039463200201500203.

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In spite of the drug's toxicity, cyclosporine A (CsA) is largely used in several diseases, including dermatological pathologies, with beneficial results. In dermatology cyclosporin-A reduces the severity of psoriasis symptoms, Bechet's disease, pyoderma gangrenosum, blistering disorders, aftous stomatitis, lichen planus, atopic dermatitis, alopecia and allergic contact dermatitis.

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15

Gelfand, E. W., R. K. Cheung, and G. B. Mills. "The cyclosporins inhibit lymphocyte activation at more than one site." Journal of Immunology 138, no. 4 (February 15, 1987): 1115–20. http://dx.doi.org/10.4049/jimmunol.138.4.1115.

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Abstract Cyclosporin A (CsA), a potent immunosuppressive agent, acts primarily by inhibiting T cell function. Although several potential sites of action have been identified, the mechanisms whereby CsA mediates its immunosuppressive properties have not been fully delineated. We have examined the effects of the immunosuppressive cyclosporins, CsA, dihydrocyclosporin D, and cyclosporin G, and a nonimmunosuppressive analog, cyclosporin H, on early events associated with activation of human T cells. Interleukin 2 (IL 2) receptor expression, as measured by immunofluorescence, was unaffected by CsA. Despite this, in the continuous presence of CsA, exogenous IL 2 did not bypass CsA inhibition of phytohemagglutinin (PHA)-induced proliferation. Thus, one site of activity of CsA is on IL 2-induced proliferation of IL 2 receptor-expressing cells. In addition, several potential mechanisms for inhibiting IL 2 secretion were identified. Changes in cytosolic free Ca2+ ([Ca2+]i), an obligatory event for PHA-induced IL 2 secretion, were inhibited by a 30-min preincubation with the immunosuppressive cyclosporins but not the inactive analog. In this action, the drug effects cannot be distinguished from that of Ca2+ channel blockers. The active compounds also resulted in membrane depolarization, an effect which may, in part, explain the reduction in PHA-induced changes in [Ca2+]i. These results identify multiple sites of action of the immunosuppressive cyclosporins, the combination of which likely accounts for their selective inhibition of T cell function in vitro and in vivo.

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16

Kobchikova, Polina P., Sergey V. Efimov, and Vladimir V. Klochkov. "Binding of Different Cyclosporin Variants to Micelles Evidenced by NMR and MD Simulations." Membranes 13, no. 2 (February 5, 2023): 196. http://dx.doi.org/10.3390/membranes13020196.

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Peptides play a critical role in the life of organisms, performing completely different functions. The biological activity of some peptides, such as cyclosporins, can be determined by the degree of membrane permeability. Thus, it becomes important to study how the molecule interacts with lipid bilayers. Cyclosporins C, E, H and L were characterised molecular dynamics simulation; NMR spectroscopy studies were also carried out for cyclosporins C and E. The comparison of one- and two-dimensional spectra revealed certain similarities between spatial structures of the studied cyclosporin variants. Upon dissolving in water containing DPC micelles, which serve as model membranes, subtle changes in the NMR spectra appear, but in a different way for different cyclosporins. In order to understand whether observed changes are related to any structural modifications, simulation of the interaction of the peptide with the phospholipid micelle was performed. The onset of the interaction was observed, when the peptide is trapped to the surface of the micelle. Simulations of this kind are also of interest in the light of the well-known membrane permeability of cyclosporin, which is important for its biological action.

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17

Riks, Inna A. "Cyclosporine use in “dry eye” syndrome." Ophthalmology journal 12, no. 3 (December 16, 2019): 75–82. http://dx.doi.org/10.17816/ov15853.

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This literature review focuses on the need for anti-inflammatory therapy for dry eye disease (DED). Causes of development and mechanisms of pathogenesis of DED are presented. Principles of action of various groups of anti-inflammatory medications, as well as recommendations for cyclosporine use of are described. The results of studies on cyclosporine efficacy are highlighted, principles of cyclosporin prescription in DED are listed.

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18

Frickhofen, Norbert, Hermann Heimpel, Joachim P. Kaltwasser, and Hubert Schrezenmeier. "Antithymocyte globulin with or without cyclosporin A: 11-year follow-up of a randomized trial comparing treatments of aplastic anemia." Blood 101, no. 4 (February 15, 2003): 1236–42. http://dx.doi.org/10.1182/blood-2002-04-1134.

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Immunosuppression with antithymocyte globulin, (methyl)prednisolone, and cyclosporin A is considered the treatment of choice for the patient with aplastic anemia without a donor for standard-risk stem cell transplantation. This consensus is supported by the results of several series, including a randomized German trial. Here we report 11-year results of the latter trial. With stringent response criteria and 4 months as the time to evaluate responses, this analysis confirms the superiority of the cyclosporine regimen regarding the response rate in all patients treated (70% vs 41%, with or without cyclosporine; P = .015) and in patients with severe aplastic anemia (65% vs 31%; P = .011). Patients responded more rapidly after treatment with cyclosporine (median, 60 vs 82 days; P = .019). Most patients treated with cyclosporine needed only one course of immunosuppression, whereas many patients treated without cyclosporine required repeated immunosuppressive treatment. Because of the efficacy of salvage treatment, overall survival was not different between the 2 treatment groups. However, failure-free survival favored the cyclosporine regimen (39% vs 24%; P = .04). The relapse rate, projected at 38% after 11.3 years, was similar between the 2 treatment groups. Remissions were cyclosporine dependent in 26% of the patients responding to a regimen that included cyclosporine. Clonal or malignant diseases developed in 25% of the patients. These data demonstrate that antithymocyte globulin, methylprednisolone, and cyclosporin A are an effective regimen for the treatment of aplastic anemia. However, remissions are unstable, and secondary diseases are common. In contrast to the results of stem cell transplantation, most patients are not cured.

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19

Anık, İhsan, M. Konuralp İlbay, Gül İlbay, Murat Yılmaz, Bedrettin Özsoy, Cengiz Erçin, and Savaş Ceylan. "Effects of Topical Cyclosporin A Application on Preventing Epineural Scar Formation in Rats: Experimental Study." Sinir Sistemi Cerrahisi Dergisi 8, no. 3 (December 21, 2022): 104–13. http://dx.doi.org/10.54306/sscd.2022.217.

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The aim of this study is to evaluate macroscopic, histopathologic and immunohistochemical effects of topical cyclosporin administration on prevention of epineural scar formation in rats.This experimental study was performed in two groups, each consisting of ten rats. Sciatic nerve was opened bilaterally. Tibial and peroneal components were set apart with blunt dissection. Abrasion injury was achieved by repetitive rubbing over biceps femoris muscle. In the control group saline sucked cotton peds were administered over opened sciatic nerve region bilaterally, whereas cyclosporin sucked peds were administered in the second group for five minutes duration. Eight weeks after surgery both groups were sacrificed and nerve complexes were evaluated microscopically, histopathologically and immunohistochemically. No side effects were observed after 5 minutes single dose topical cyclosporine administration in our study. Cutaneous, muscular and deep fascial repairment were almost completed according to Petersen’s numerical grading system (p<0.05). Nerve adherence was significantly decreased (p<0.001) in the ones treated with cyclosporin than the control group. FGF expression was demonstrated and individual evaluations of the control and the study groups immunhistochemically. The ratio of fibroblast/fibrosit number showed that both groups results were parallel. Single dose topical cyclosporin administration is shown to be successfull in preventing epineural scar formation after peripheric nerve neurolysis.

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20

&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 694 (March 1998): 8. http://dx.doi.org/10.2165/00128415-199806940-00023.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 709 (July 1998): 5–6. http://dx.doi.org/10.2165/00128415-199807090-00016.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 711 (July 1998): 7. http://dx.doi.org/10.2165/00128415-199807110-00022.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 714 (August 1998): 7. http://dx.doi.org/10.2165/00128415-199807140-00022.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 714 (August 1998): 8. http://dx.doi.org/10.2165/00128415-199807140-00028.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 715 (August 1998): 7. http://dx.doi.org/10.2165/00128415-199807150-00019.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 727 (November 1998): 7–8. http://dx.doi.org/10.2165/00128415-199807270-00018.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 732 (December 1998): 8. http://dx.doi.org/10.2165/00128415-199807320-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 734 (January 1999): 7. http://dx.doi.org/10.2165/00128415-199907340-00016.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 735 (January 1999): 7. http://dx.doi.org/10.2165/00128415-199907350-00016.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 742 (March 1999): 6–7. http://dx.doi.org/10.2165/00128415-199907420-00015.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 751 (May 1999): 7. http://dx.doi.org/10.2165/00128415-199907510-00022.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 752 (May 1999): 8. http://dx.doi.org/10.2165/00128415-199907520-00026.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 753 (May 1999): 8. http://dx.doi.org/10.2165/00128415-199907530-00027.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 757 (June 1999): 8. http://dx.doi.org/10.2165/00128415-199907570-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 760 (July 1999): 7. http://dx.doi.org/10.2165/00128415-199907600-00018.

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&NA;. "Cyclosporin." Inpharma Weekly &NA;, no. 1174 (February 1999): 20. http://dx.doi.org/10.2165/00128413-199911740-00038.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 535 (January 1995): 6. http://dx.doi.org/10.2165/00128415-199505350-00020.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 538 (February 1995): 7. http://dx.doi.org/10.2165/00128415-199505380-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 539 (February 1995): 7. http://dx.doi.org/10.2165/00128415-199505390-00019.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 546 (April 1995): 6. http://dx.doi.org/10.2165/00128415-199505460-00017.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 547 (April 1995): 5. http://dx.doi.org/10.2165/00128415-199505470-00011.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 548 (April 1995): 7. http://dx.doi.org/10.2165/00128415-199505480-00023.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 551 (May 1995): 6. http://dx.doi.org/10.2165/00128415-199505510-00023.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 554 (June 1995): 6. http://dx.doi.org/10.2165/00128415-199505540-00021.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 556 (June 1995): 7. http://dx.doi.org/10.2165/00128415-199505560-00025.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 557 (July 1995): 5. http://dx.doi.org/10.2165/00128415-199505570-00015.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 563 (August 1995): 6. http://dx.doi.org/10.2165/00128415-199505630-00017.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 564 (August 1995): 6. http://dx.doi.org/10.2165/00128415-199505640-00015.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 567 (September 1995): 5. http://dx.doi.org/10.2165/00128415-199505670-00012.

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&NA;. "Cyclosporin." Reactions Weekly &NA;, no. 569 (September 1995): 7. http://dx.doi.org/10.2165/00128415-199505690-00017.

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