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Published: 10 December 2022
Last updated: 29 January 2023

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1

Moyer, Paula. "Muramyl tripeptide for treatment of osteosarcoma." Lancet Oncology 9, no. 3 (March 2008): 207. http://dx.doi.org/10.1016/s1470-2045(08)70057-3.

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2

Silverman, D. H., J. M. Krueger, and M. L. Karnovsky. "Specific binding sites for muramyl peptides on murine macrophages." Journal of Immunology 136, no. 6 (March 15, 1986): 2195–201. http://dx.doi.org/10.4049/jimmunol.136.6.2195.

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Abstract Two radiolabeled (125I) muramyl peptide derivatives of high specific activity were prepared: a tripeptide with an iodinated C-terminal tyrosine methyl ester (Ligand I), and a muramyl tripeptide with a C-terminal lysine derivatized with Bolton-Hunter reagent (Ligand II). These were used to characterize binding of muramyl peptides to monolayers of murine macrophages. Saturable high-affinity binding to resident, caseinate-elicited, and Listeria-activated peritoneal cells was observed with both radioligands. Binding affinities varied with the state of activation of the macrophages, and KD values ranged from 48 +/- 33 pM (for resident macrophages, Ligand I) to 1020 +/- 90 pM (for activated macrophages, Ligand II). Specific binding sites were also found on a macrophage-derived cell line. The ability of several unlabeled muramyl peptides to compete with Ligands I and II for their binding sites was tested. Competition was stereospecific and correlated with known biological activities of these compounds (i.e., immunoadjuvanticity, pyrogenicity, and somnogenicity). The sites identified here for Ligands I and II may mediate some of the effects that muramyl peptides have previously been demonstrated to have on macrophages.
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3

Meyers, Paul A. "Muramyl tripeptide (mifamurtide) for the treatment of osteosarcoma." Expert Review of Anticancer Therapy 9, no. 8 (August 2009): 1035–49. http://dx.doi.org/10.1586/era.09.69.

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4

Goldbach, P., S. Dumont, R. Kessler, P. Poindron, and A. Stamm. "In situ activation of mouse alveolar macrophages by aerosolized liposomal IFN-gamma and muramyl tripeptide." American Journal of Physiology-Lung Cellular and Molecular Physiology 270, no. 3 (March 1, 1996): L429—L434. http://dx.doi.org/10.1152/ajplung.1996.270.3.l429.

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Interferon-gamma (IFN-gamma) was entrapped with an efficiency of 30-40% in muramyl tripeptide-containing liposomes by a freeze-thawing procedure. A microcytotoxicity assay was developed to measure the tumoricidal activity of mouse alveolar macrophages (AM) against tumoral target cells with a colorimetric viability test. Free IFN-gamma and liposomal muramyl tripeptide phosphatidylethanolamine (MTP-PE) were found to be only slightly effective to activate in vitro AM, whereas encapsulation of both INF-gamma and MTP-PE within the same liposomes produced higher activation of AM. Aerosolized IFN-gamma and liposomal immunomodulators enhanced antitumor properties of AM recovered in mice 24 h postinhalation. Whereas free IFN-gamma also induced a substantial activation of peritoneal macrophages, liposomal encapsulation significantly reduced the systemic activity of inhaled immunomodulators. This approach provides a useful model for the compartmentalized organ-specific activation of AM in mice.
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5

Kleinerman, Eugenie S. "Biologic Therapy for Osteosarcoma Using Liposome-Encapsulated Muramyl Tripeptide." Hematology/Oncology Clinics of North America 9, no. 4 (August 1995): 927–38. http://dx.doi.org/10.1016/s0889-8588(18)30079-0.

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6

Kleinerman, Eugenie S., Paul A. Meyers, Austin K. Raymond, Jacalyn B. Gano, Shu-Fang Jia, and Norman Jaffe. "Combination Therapy with Ifosfamide and Liposome-Encapsulated Muramyl Tripeptide." Journal of Immunotherapy 17, no. 2 (April 1995): 181–93. http://dx.doi.org/10.1097/00002371-199504000-00007.

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7

Anderson, Peter. "Liposomal muramyl tripeptide phosphatidyl ethanolamine: ifosfamide-containing chemotherapy in osteosarcoma." Future Oncology 2, no. 3 (June 2006): 333–43. http://dx.doi.org/10.2217/14796694.2.3.333.

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8

Murray, J. L., E. S. Kleinerman, J. E. Cunningham, J. R. Tatom, K. Andrejcio, J. Lepe-Zuniga, L. M. Lamki, M. G. Rosenblum, H. Frost, and J. U. Gutterman. "Phase I trial of liposomal muramyl tripeptide phosphatidylethanolamine in cancer patients." Journal of Clinical Oncology 7, no. 12 (December 1989): 1915–25. http://dx.doi.org/10.1200/jco.1989.7.12.1915.

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Twenty-eight evaluable patients with metastatic cancer refractory to standard therapy received escalating doses of muramyl tripeptide phosphatidylethanolamine (MTP-PE) (.05 to 12 mg/m2) in phosphatidylserine (PC):phosphatidylcholine (PS) liposomes (lipid:MTP-PE) ratio 250:1). Liposomal MTP-PE (L-MTP-PE) was infused over 1 hour twice weekly; doses were escalated within individual patients every 3 weeks as tolerated for a total treatment duration of 9 weeks. Routine clinical laboratory parameters, acute phase reactants and various immunologic tests were monitored at various time points during treatment. Toxicity was moderate (less than or equal to grade II) in 24 patients with chief side effects being chills (80% of patients), fever (70%), malaise (60%), and nausea (55%). In four patients L-MTP-PE treatment was deescalated due to severe malaise and recurrent fever higher than 38.8 degrees C. The maximum-tolerated dose (MTD) was 6 mg/m2. Significant (P less than .05) increases in WBC count, absolute granulocyte count, ceruloplasmin, beta 2-microglobulin, c-reactive protein, monocyte tumoricidal activity, and serum IL-1 beta were found. Significant decreases in serum cholesterol were also observed. Clearance of intravenously (iv)-infused technetium-99 (99mTc)-labeled liposomes containing MTP-PE in four patients was biphasic; gamma camera scans revealed uptake of radiolabel in liver, spleen, lung, nasopharynx, thyroid gland, and tumor (two patients). No objective tumor regression was seen. In view of its definite immunobiologic activity and lack of major toxicity, additional phase II and adjuvant trials of L-MTP-PE are warranted.
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9

Gay, B., H. Towbin, C. Schnell, K. Einsle, P. Graf, and D. Gygax. "Direct chemiluminescence immunoassay (CLIA) for muramyl tripeptide phosphatidyl-ethanolamine in plasma." Journal of Bioluminescence and Chemiluminescence 6, no. 2 (April 1991): 73–80. http://dx.doi.org/10.1002/bio.1170060204.

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10

Karpoff, Howard M., William Jarnagin, Keith Delman, and Yuman Fong. "Regional muramyl tripeptide phosphatidylethanolamine administration enhances hepatic immune function and tumor surveillance." Surgery 128, no. 2 (August 2000): 213–18. http://dx.doi.org/10.1067/msy.2000.107420.

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11

Fedoročko, P. "Liposomal Muramyl Tripeptide Phosphatidylethanolamine (MTP-PE) Promotes Haemopoietic Recovery in Irradiated Mouse." International Journal of Radiation Biology 65, no. 4 (January 1994): 465–75. http://dx.doi.org/10.1080/09553009414550541.

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12

Fogler, W. E., R. Wade, D. E. Brundish, and I. J. Fidler. "Distribution and fate of free and liposome-encapsulated [3H]nor-muramyl dipeptide and [3H]muramyl tripeptide phosphatidylethanolamine in mice." Journal of Immunology 135, no. 2 (August 1, 1985): 1372–77. http://dx.doi.org/10.4049/jimmunol.135.2.1372.

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Abstract The pharmacokinetics and metabolism of i.v. administered free (unencapsulated) or liposome-encapsulated hydrophilic [3H]-labeled nor-muramyl dipeptide (nor-MDP) and lipophilic [3H]-labeled muramyl tripeptide phosphatidylethanolamine (MTP-PE) were evaluated. In addition we also examined the distribution and fate of these immunomodulators subsequent to intranasal (i.n.) administration. Unique patterns of circulatory clearance, organ distribution, metabolism, and excretion were observed for each of the four preparations. Nor-MDP in saline was rapidly cleared from the circulation and excreted in the urine as intact molecules. MTP-PE dissolved in saline was cleared from the circulation at a slow rate and found within various organs as intact MTP-PE, lyso-MTP-PE, and MDP. Following the i.v. administration of nor-MDP or MTP-PE in liposomes, patterns of clearance and organ distribution corresponded to that of liposome distribution, i.e., the reticuloendothelial system. Extensive dissociation of hydrophilic nor-MDP from the carrier liposomes occurred, and the immunomodulator was recovered in the urine. In contrast, MTP-PE entrapped in liposomes was retained in target organs for the duration of the study. The i.n. instillation of radiolabeled nor-MDP or MTP-PE was associated with the accumulation of these immunomodulators in the brain. Our results demonstrate the feasibility of targeting hydrophilic and lipophilic immunomodulators to cells of the macrophage-histiocyte series.
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13

Sobral, R. G., A. M. Ludovice, H. de Lencastre, and A. Tomasz. "Role of murF in Cell Wall Biosynthesis: Isolation and Characterization of a murF Conditional Mutant of Staphylococcus aureus." Journal of Bacteriology 188, no. 7 (April 1, 2006): 2543–53. http://dx.doi.org/10.1128/jb.188.7.2543-2553.2006.

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ABSTRACT The Staphylococcus aureus murF gene was placed under the control of a promoter inducible by IPTG (isopropyl-β-d-thiogalactopyranoside). It was demonstrated that murF is an essential gene; it is cotranscribed with ddlA and growth rate, level of beta-lactam antibiotic resistance, and rates of transcription of the mecA and pbpB genes paralleled the rates of transcription of murF. At suboptimal concentrations of the inducer, a UDP-linked muramyl tripeptide accumulated in the cytoplasm in parallel with the decline in the amounts of the normal pentapeptide cell wall precursor. The abnormal tripeptide component incorporated into the cell wall as a monomeric muropeptide, accompanied by a decrease in the oligomerization degree of the peptidoglycan. However, incorporation of the tripeptide into the cell wall was limited to a relatively low threshold value. Further reduction of the amounts of pentapeptide cell wall precursor caused a gradual decrease in the cellular amounts of peptidoglycan, the production of a thinner peripheral cell wall, aberrant septae, and an overall increase in the diameter of the cells. The observations suggest that the role of murF exceeds its primary function in peptidoglycan biosynthesis and may also be involved in the control of cell division.
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14

Fogler, William E., and Isaiah J. Fidler. "Comparative interaction of free and liposome-encapsulated nor-muramyl dipeptide or muramyl tripeptide phosphatidylethanolamine (3H-labelled) with human blood monocytes." International Journal of Immunopharmacology 9, no. 2 (January 1987): 141–50. http://dx.doi.org/10.1016/0192-0561(87)90088-9.

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15

Nardin, A., M. Lefebvre, K. Labroquere, O. Faure, and J. Abastado. "Liposomal Muramyl Tripeptide Phosphatidylethanolamine: Targeting and Activating Macrophages for Adjuvant Treatment of Osteosarcoma." Current Cancer Drug Targets 6, no. 2 (March 1, 2006): 123–33. http://dx.doi.org/10.2174/156800906776056473.

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16

Kleinerman, Eugenie S., Jacalyn B. Gano, Dennis A. Johnston, Robert S. Benjamin, and Norman Jaffe. "Efficacy of Liposomal Muramyl Tripeptide (CGP 19835A) in the Treatment of Relapsed Osteosarcoma." American Journal of Clinical Oncology 18, no. 2 (April 1995): 93–99. http://dx.doi.org/10.1097/00000421-199504000-00001.

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17

MacEwen, E. G., I. D. Kurzman, R. C. Rosenthal, B. W. Smith, P. A. Manley, J. K. Roush, and P. E. Howard. "Therapy for Osteosarcoma in Dogs With Intravenous Injection of Liposome-Encapsulated Muramyl Tripeptide." JNCI Journal of the National Cancer Institute 81, no. 12 (June 21, 1989): 935–38. http://dx.doi.org/10.1093/jnci/81.12.935.

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18

Jarowenko, Daleela Getsiv, Scott C. Sigler, and Neal R. Pellis. "Muramyl tripeptide: An effective immunotherapy in the surgical setting for pediatric abdominal neoplasms." Journal of Pediatric Surgery 22, no. 6 (June 1987): 497–500. http://dx.doi.org/10.1016/s0022-3468(87)80204-x.

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19

Chou, Alexander J., Eugenie S. Kleinerman, Mark D. Krailo, Zhengjia Chen, Donna L. Betcher, John H. Healey, Ernest U. Conrad, et al. "Addition of muramyl tripeptide to chemotherapy for patients with newly diagnosed metastatic osteosarcoma." Cancer 115, no. 22 (July 27, 2009): 5339–48. http://dx.doi.org/10.1002/cncr.24566.

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20

Mori, Kanji, Kosei Ando, and Dominique Heymann. "Liposomal muramyl tripeptide phosphatidyl ethanolamine: a safe and effective agent against osteosarcoma pulmonary metastases." Expert Review of Anticancer Therapy 8, no. 2 (February 2008): 151–59. http://dx.doi.org/10.1586/14737140.8.2.151.

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21

Galligionl, E., M. Quaia, A. Freschi, A. Spada, D. Favaro, M. Sanarosa, C. Sacco, and D. Alberti. "Biological and clinical activity of liposomes containing muramyl tripeptide LMTP-PE on melanoma patients." Melanoma Research 3, no. 1 (March 1993): 76. http://dx.doi.org/10.1097/00008390-199303000-00282.

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22

Ding, Jin Wen, Roland Andersson, Vasile L. Soltesz, Håkan Pärsson, Kjell Johansson, Wenqi Wang, and Stig Bengmark. "Inhibition of bacterial translocation in obstructive jaundice by muramyl tripeptide phosphatidylethanolamine in the rat." Journal of Hepatology 20, no. 6 (January 1994): 720–28. http://dx.doi.org/10.1016/s0168-8278(05)80141-2.

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23

Calvo-Mateo, Ana, María-José Camarasa, and Federico G. De las Heras. "N-(glucopyranosid-3-yl)--alanyl--alanyl--isoglutamine and related tripeptide analogues of muramyl dipeptide." Tetrahedron 42, no. 14 (January 1986): 4049–56. http://dx.doi.org/10.1016/s0040-4020(01)87561-x.

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24

Maeda, Miho, Takeshi Asano, and Eugenie S. Kleinerman. "Anti-(tumor necrosis factor) alters the response of human monocytes to liposomal muramyl tripeptide." Cancer Immunology Immunotherapy 37, no. 3 (May 1993): 203–8. http://dx.doi.org/10.1007/bf01525436.

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25

Taçyıldız, Nurdan, Emel Unal, Handan Dinçaslan, H. Mine Çakmak, Kenan Köse, Gülşah Tanyıldız, and Ömer Kartal. "Muramyl Tripeptide Plus Chemotherapy Reduces Metastasis in Non-Metastatic Osteosarcoma: A Single-Center Experience." Asian Pacific Journal of Cancer Prevention 21, no. 3 (March 1, 2020): 715–20. http://dx.doi.org/10.31557/apjcp.2020.21.3.715.

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26

Izbicki, J. R., C. Raedler, A. Anke, P. Brunner, M. Siebeck, E. Leinisch, R. Lüttiken, G. Ruckdeschel, D. K. Wilker, and L. Schweiberer. "Beneficial effect of liposome-encapsulated muramyl tripeptide in experimental septicemia in a porcine model." Infection and Immunity 59, no. 1 (1991): 126–30. http://dx.doi.org/10.1128/iai.59.1.126-130.1991.

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27

Shaw, J. M., W. S. Futch, and L. B. Schook. "Induction of macrophage antitumor activity by acetylated low density lipoprotein containing lipophilic muramyl tripeptide." Proceedings of the National Academy of Sciences 85, no. 16 (August 1, 1988): 6112–16. http://dx.doi.org/10.1073/pnas.85.16.6112.

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28

Melissen, P. M., W. van Vianen, Y. Rijsbergen, and I. A. Bakker-Woudenberg. "Free versus liposome-encapsulated muramyl tripeptide phosphatidylethanolamide in treatment of experimental Klebsiella pneumoniae infection." Infection and Immunity 60, no. 1 (1992): 95–101. http://dx.doi.org/10.1128/iai.60.1.95-101.1992.

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29

Favaro, D., M. Santarosa, M. Quaia, A. Spada, A. Freschi, R. Talmini, and E. Galligioni. "Soluble intercellular adhesion molecule-1 in melanoma patients treated with liposomes containing muramyl tripeptide." European Journal of Cancer 31, no. 6 (June 1995): 1026–27. http://dx.doi.org/10.1016/0959-8049(95)00118-2.

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30

Gay, Brigitte, Jean-Michel Cardot, Christian Schnell, Peter Van Hoogevest, and Daniel Gygax. "Comparative Pharmacokinetics of Free Muramyl Tripeptide Phosphatidyl Ethanolamine (MTP-PE) and Liposomal MTP-PE." Journal of Pharmaceutical Sciences 82, no. 10 (October 1993): 997–1001. http://dx.doi.org/10.1002/jps.2600821005.

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31

Dalmasso, Guillaume, Hang Thi Thu Nguyen, Laetitia Charrier-Hisamuddin, Yutao Yan, Hamed Laroui, Benjamin Demoulin, Shanthi V. Sitaraman, and Didier Merlin. "PepT1 mediates transport of the proinflammatory bacterial tripeptide l-Ala-γ-d-Glu-meso-DAP in intestinal epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 299, no. 3 (September 2010): G687—G696. http://dx.doi.org/10.1152/ajpgi.00527.2009.

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PepT1 is a di/tripeptide transporter highly expressed in the small intestine, but poorly or not expressed in the colon. However, during chronic inflammation, such as inflammatory bowel disease, PepT1 expression is induced in the colon. Commensal bacteria that colonize the human colon produce a large amount of di/tripeptides. To date, two bacterial peptides ( N-formylmethionyl-leucyl-phenylalanine and muramyl dipeptide) have been identified as substrates of PepT1. We hypothesized that the proinflammatory tripeptide l-Ala-γ-d-Glu- meso-DAP (Tri-DAP), a breakdown product of bacterial peptidoglycan, is transported into intestinal epithelial cells via PepT1. We found that uptake of glycine-sarcosine, a specific substrate of PepT1, in intestinal epithelial Caco2-BBE cells was inhibited by Tri-DAP in a dose-dependent manner. Tri-DAP induced activation of NF-κB and MAP kinases, consequently leading to production of the proinflammatory cytokine interleukin-8. Tri-DAP-induced inflammatory response in Caco2-BBE cells was significantly suppressed by silencing of PepT1 expression by using PepT1-shRNAs in a tetracycline-regulated expression ( Tet-off) system. Colonic epithelial HT29-Cl.19A cells, which do not express PepT1 under basal condition, were mostly insensitive to Tri-DAP-induced inflammation. However, HT29-Cl.19A cells exhibited proinflammatory response to Tri-DAP upon stable transfection with a plasmid encoding PepT1. Accordingly, Tri-DAP significantly increased keratinocyte-derived chemokine production in colonic tissues from transgenic mice expressing PepT1 in intestinal epithelial cells. Finally, Tri-DAP induced a significant drop in intracellular pH in intestinal epithelial cells expressing PepT1, but not in cells that did not express PepT1. Our data collectively support the classification of Tri-DAP as a novel substrate of PepT1. Given that PepT1 is highly expressed in the colon during inflammation, PepT1-mediated Tri-DAP transport may occur more effectively during such conditions, further contributing to intestinal inflammation.
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32

MacEwen, E. Gregory, Fushun Shi, and Ilene D. Kurzman. "IN VIVO EFFECT OF CHEMOTHERAPY COMBINED WITH LIPOSOME-ENCAPSULATED MURAMYL TRIPEPTIDE ON CANINE MONOCYTE ACTIVATION." Journal of Immunotherapy 13, no. 1 (January 1993): 65. http://dx.doi.org/10.1097/00002371-199301000-00036.

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33

Koff, W., S. Showalter, B. Hampar, and I. Fidler. "Protection of mice against fatal herpes simplex type 2 infection by liposomes containing muramyl tripeptide." Science 228, no. 4698 (April 26, 1985): 495–97. http://dx.doi.org/10.1126/science.2984772.

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34

Verweij, J., I. Judson, W. Steward, C. A. van Oosterom. van Pottelsberghe, M. van Glabbeke, and H. Mouridsen. "Phase II study with liposomal muramyl tripeptide phophatidylethanolamine (MTP/PE) in soft tissue sarcomas (STS)." European Journal of Cancer 29 (January 1993): S184. http://dx.doi.org/10.1016/0959-8049(93)91647-4.

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35

Barr, P. J., K. M. Green, H. L. Gibson, I. C. Bathurst, I. A. Quakyi, and D. C. Kaslow. "Recombinant Pfs25 protein of Plasmodium falciparum elicits malaria transmission-blocking immunity in experimental animals." Journal of Experimental Medicine 174, no. 5 (November 1, 1991): 1203–8. http://dx.doi.org/10.1084/jem.174.5.1203.

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Pfs25 is a sexual stage antigen of Plasmodium falciparum that is expressed on the surface of zygote and ookinete forms of the parasite. Monoclonal antibodies directed against native Pfs25 can block completely the development of P. falciparum oocysts in the midgut of the mosquito vector. Thus, this 25-kD protein is a potential vaccine candidate for eliciting transmission-blocking immunity in inhabitants of malaria endemic regions. We have synthesized, by secretion from yeast, a polypeptide analogue of Pfs25 that reacts with conformation-dependent monoclonal antibodies, and elicits transmission-blocking antibodies when used to immunize mice and monkeys in conjunction with a muramyl tripeptide adjuvant. Our results suggest the further evaluation of recombinant DNA-derived Pfs25 in transmission-blocking vaccination studies in humans.
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36

Tanaka, Motoharu, and Shigeru Abe. "Combination therapy of liposome-entrapped muramyl tripeptide phosphatidylethanolamine (L-MTP-PE) against syngeneic tumors in mice." Proceedings for Annual Meeting of The Japanese Pharmacological Society 93 (2020): 3—P—344. http://dx.doi.org/10.1254/jpssuppl.93.0_3-p-344.

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37

Melissen, P. M., W. van Vianen, and I. A. Bakker-Woudenberg. "Treatment of Klebsiella pneumoniae septicemia in normal and leukopenic mice by liposome-encapsulated muramyl tripeptide phosphatidylethanolamide." Antimicrobial Agents and Chemotherapy 38, no. 1 (January 1, 1994): 147–50. http://dx.doi.org/10.1128/aac.38.1.147.

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38

Kleinerman, E. S., J. S. Snyder, and N. Jaffe. "Influence of chemotherapy administration on monocyte activation by liposomal muramyl tripeptide phosphatidylethanolamine in children with osteosarcoma." Journal of Clinical Oncology 9, no. 2 (February 1991): 259–67. http://dx.doi.org/10.1200/jco.1991.9.2.259.

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The purpose of these studies was to determine whether chemotherapy interfered with the ability of peripheral blood monocytes from patients with osteosarcoma to respond to the liposome-encapsulated activating agent muramyl tripeptide phosphatidylethanolamine (L-MTP-PE). This was done in preparation of designing an adjuvant therapy protocol that includes L-MTP-PE combined with chemotherapy postoperatively for the treatment of primary osteosarcoma. The majority of patients who fail current adjuvant chemotherapy do so while on chemotherapy. Therefore, we believe it is important to combine L-MTP-PE with chemotherapy early in the treatment course rather than waiting until all chemotherapy cycles are completed. The tumoricidal properties of monocytes from patients with osteosarcoma could be activated by L-MTP-PE to levels equal to or greater than those expressed by normal control monocytes. No intrinsic monocyte defect could be demonstrated. Single-agent chemotherapy consisting of cisplatin (CPD), high-dose methotrexate (MTX), Cytoxan (CTX, cyclophosphamide; Bristol-Myers Co, Evansville, IN), or Adriamycin (ADR, doxorubicin; Adria Laboratories, Columbus, OH) did not interfere with this activation process. There was even a suggestion of enhanced activation potential following the administration of ADR. However, when both ADR and CTX were administered together on the same day, profound suppression in monocyte activation was observed. This suppressed function returned to normal by 3 weeks postcombination therapy. We therefore conclude that L-MTP-PE can be combined with ADR, CPD, MTX, or CTX as single agents but recommend that ADR plus L-MTP-PE is the most effective combination. By contrast, we discourage the use of L-MTP-PE when ADR and CTX are given together.
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39

Favaro, Daniela, Manuela Santarosa, Michele Quaia, Antonella Spada, Andrea Freschi, Renato Talamini, and Enzo Galligioni. "Soluble Intercellular Adhesion Molecule-1 and Serum Cytokines in Melanoma Patients Treated with Liposomes Containing Muramyl Tripeptide." Tumori Journal 81, no. 3 (May 1995): 185–90. http://dx.doi.org/10.1177/030089169508100306.

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Aims and Background A soluble form of intercellular adhesion molecule-1 (sICAM-1) has been recently identified in patients with malignant melanoma. It has been demonstrated that inflammatory cytokines can modulate the cellular expression of ICAM-1 and the shedding of this molecule by cells. To our knowledge, few data exist on serum sICAM-1 levels in cancer patients treated with immunomodulators. Liposomes containing muramyl tripeptide (MLV MTP-PE) can activate monocytes from cancer patients in vitro and in vivo, making them cytotoxic such as tumor necrosis factor- α (TNF-α) and Interleukin-6 (IL-6). The purpose of the present study was to evaluate the levels of sICAM-1 and their possible correlation with serum inflammatory cytokine levels in melanoma patients treated with MLV MTP-PE. Methods The sera from 9 patients with metastatic melanoma treated with MLV MTP-PE, 4 mg i.v. twice a week for 12 weeks, were tested in ELISA system to detect sICAM-1, TNF-α, IL-6, Interleukin-1 β (IL- β) and Interferon-γ (IFN-γ) before, and 2 and 24 h after the 1st, 12th and 24th infusion of MLV MTP-PE. Results Baseline levels of sICAM-1 were elevated in all patients (median 540 ng/ml: range 400-1030 ng/ml). Twenty-four h after the 1st infusion of MLV MTP-PE, we observed 6 increases in sICAM-1 levels, 1 decrease and 2 stable values (median 720 ng/ml: range 410-1820; P = 0.060). Twenty-four h after the 12th infusion, sICAM-1 increased in 3 patients and did not change in 4 (median 790 ng/ml: range 495-1650 ng/ml; P = 0.069). At the 24th infusion, sICAM-1 increased in 4 of 6 evaluable patients and remained stable in 2 (median 802 ng/ml: range 510-1450 ng/ml; P = 0.045). To better analyze the variations in sICAM-1, the patients were arbitrarily divided into two groups according to their clinical behavior: 4 presented stabilization (all lesions, n = 2; some lesions, n = 2) (Group A); 5 presented progressive disease (Group B). In Group A, sICAM-1 levels remained stable or showed a modest increase during treatment (except in 1 patient, who exhibited a substantial variation after the 12th infusion). In contrast, in Group B very high levels of sICAM-1 were observed at the beginning of the study therapy in 1 patient and after the 1st infusion in 3 patients; these values remained high until the 24th infusion. In most of the patients, TNF-α and IL-6 increased after the 1st infusion, but not thereafter. IFN-γ was never detected; IL-1 β was detectable in a few cases, but only before the infusions. Conclusions baseline levels of sICAM-1 were elevated in all patients and further increased during treatment only in patients with more aggressive disease. No correlation was found between sICAM-1 and inflammatory cytokines. It would therefore seem that in patients with advanced disease, higher levels and a progressive increase in sICAM-1 may be unfavorable prognostic factors.
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Kurzman, Ilene D., Haiyan Cheng, and E. Gregory MacEwen. "Effect of Liposome-Muramyl Tripeptide Combined with Recombinant Canine Granulocyte Colony-Stimulating Factor on Canine Monocyte Activity." Cancer Biotherapy 9, no. 2 (January 1994): 113–22. http://dx.doi.org/10.1089/cbr.1994.9.113.

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Kleinerman, E. S., S. F. Jia, J. Griffin, N. L. Seibel, R. S. Benjamin, and N. Jaffe. "Phase II study of liposomal muramyl tripeptide in osteosarcoma: the cytokine cascade and monocyte activation following administration." Journal of Clinical Oncology 10, no. 8 (August 1992): 1310–16. http://dx.doi.org/10.1200/jco.1992.10.8.1310.

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PURPOSE A phase II trial that uses liposome-encapsulated muramyl tripeptide phosphatidylethanolamine (L-MTP-PE) in patients with relapsed osteosarcoma is underway. To determine if in vivo cytokine induction plays a role in the mechanism of action of L-MTP-PE, we investigated the circulating cytokine levels of 16 patients who were undergoing therapy. PATIENTS AND METHODS Patients had histologically proven osteosarcoma and pulmonary metastases that developed either during adjuvant chemotherapy or that were present at diagnosis and persisted despite chemotherapy. Patients were rendered disease-free by surgery. The major goal of the study was to improve the disease-free interval in this high-risk group. L-MTP-PE 2 mg/m2 was infused during a 1-hour period twice a week for 12 weeks, then once a week for 12 weeks. Serial blood samples were collected after L-MTP-PE administration and were assayed for cytokine levels (tumor necrosis factor-alpha [TNF alpha] interleukin-1 alpha [IL-1 alpha], IL-1 beta, IL-6, interferon-gamma [IFN-gamma], neopterin, C-reactive protein). RESULTS After the infusion of L-MTP-PE, there was rapid induction of circulating TNF alpha and IL-6. TNF alpha levels peaked 1 to 2 hours after infusion in 10 of 16 patients, whereas peak IL-6 levels were detected at 2 to 3 hours in all patients. Induction of circulating TNF alpha and IL-6 was evident only after the first dose of L-MTP-PE. Neither IL-1 alpha nor IL-1 beta was detected in the plasma. Neopterin levels increased at 24 hours postinfusion, which indicated macrophage activation, and were not related to the induction of circulating IFN-gamma. C-reactive protein was elevated in all patients at 24 hours and decreased by 72 hours. Unlike circulating TNF alpha and IL-6, elevations in C-reactive protein and neopterin could be detected throughout the treatment course. CONCLUSION It is concluded that L-MTP-PE has specific biologic effects in patients with osteosarcoma that may be important to the drug's immunostimulatory capacity and its effectiveness as an antitumor agent.
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Miwa, Shinji, Toshiharu Shirai, Norio Yamamoto, Katsuhiro Hayashi, Akihiko Takeuchi, Kentaro Igarashi, and Hiroyuki Tsuchiya. "Current and Emerging Targets in Immunotherapy for Osteosarcoma." Journal of Oncology 2019 (January 1, 2019): 1–8. http://dx.doi.org/10.1155/2019/7035045.

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Osteosarcoma is the most common primary malignancy of bone. Although outcomes of patients with osteosarcoma have improved since the introduction of chemotherapy, outcomes of metastatic or unresectable osteosarcomas are still unsatisfactory. To improve osteosarcoma outcomes, the development of novel systemic therapies for osteosarcoma is needed. Since the 1880s, various immunotherapies have been utilized in patients with osteosarcoma and some patients have shown response to the treatment. Based on recent studies about the role of the immune system in malignancies, immunotherapies including immune modulators such as interleukin-2 and muramyl tripeptide, dendritic cells, immune checkpoint inhibitors, and engineered T cells have been utilized in patients with malignancies. Although there are limited reports of immunotherapies for osteosarcoma, immunotherapy is thought to be a promising treatment option for treating osteosarcomas. In this review, an overview of various immunotherapies for osteosarcoma is provided and their potential as adjuvant therapies is discussed.
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43

Mahapatra, Sebabrata, Hataichanok Scherman, Patrick J. Brennan, and Dean C. Crick. "N Glycolylation of the Nucleotide Precursors of Peptidoglycan Biosynthesis of Mycobacterium spp. Is Altered by Drug Treatment." Journal of Bacteriology 187, no. 7 (April 1, 2005): 2341–47. http://dx.doi.org/10.1128/jb.187.7.2341-2347.2005.

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ABSTRACT The peptidoglycan of Mycobacterium spp. reportedly has some unique features, including the occurrence of N-glycolylmuramic rather than N-acetylmuramic acid. However, very little is known of the actual biosynthesis of mycobacterial peptidoglycan, including the extent and origin of N glycolylation. In the present work, we have isolated and analyzed muramic acid residues located in peptidoglycan and UDP-linked precursors of peptidoglycan from Mycobacterium tuberculosis and Mycobacterium smegmatis. The muramic acid residues isolated from the mature peptidoglycan of both species were shown to be a mixture of the N-acetyl and N-glycolyl derivatives, not solely the N-glycolylated product as generally reported. The isolated UDP-linked N-acylmuramyl-pentapeptide precursor molecules also contain a mixture of N-acetyl and N-glycolyl muramyl residues in apparent contrast to previous observations in which the precursors isolated after treatment with d-cycloserine consisted entirely of N-glycolyl muropeptides. However, nucleotide-linked peptidoglycan precursors isolated from M. tuberculosis treated with d-cycloserine contained only N-glycolylmuramyl-tripeptide precursors, whereas those from similarly treated M. smegmatis consisted of a mixture of N-glycolylated and N-acetylated residues. The full pentapeptide intermediate, isolated following vancomycin treatment of M. smegmatis, consisted of the N-glycolyl derivative only, whereas the corresponding M. tuberculosis intermediate was a mixture of both the N-glycolyl and N-acetyl products. Thus, treatment with vancomycin and d-cylcoserine not only caused an accumulation of nucleotide-linked intermediate compounds but also altered their glycolylation status, possibly by altering the normal equilibrium maintained by de novo biosynthesis and peptidoglycan recycling.
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Macewen, E. G., I. D. Kurzman, S. Helfand, D. Vail, C. London, W. Kisseberth, R. C. Rosenthal, et al. "Current Studies of Liposome Muramyl Tripeptide (CGP 19835A Lipid) Therapy for Metastasis in Spontaneous Tumors: A Progress Review*." Journal of Drug Targeting 2, no. 5 (January 1994): 391–96. http://dx.doi.org/10.3109/10611869408996814.

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Maeda, Miho, Rebecca D. Knowles, and Eugenie S. Kleinerman. "Muramyl Tripeptide Phosphatidylethanolamine Encapsulated in Liposomes Stimulates Monocyte Production of Tumor Necrosis Factor and Interleukin-1 In Vitro." Cancer Communications 3, no. 10 (January 1, 1991): 313–21. http://dx.doi.org/10.3727/095535491820873740.

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46

Meyers, Paul A., Cindy L. Schwartz, Mark D. Krailo, John H. Healey, Mark L. Bernstein, Donna Betcher, William S. Ferguson, et al. "Osteosarcoma: The Addition of Muramyl Tripeptide to Chemotherapy Improves Overall Survival—A Report From the Children's Oncology Group." Journal of Clinical Oncology 26, no. 4 (February 1, 2008): 633–38. http://dx.doi.org/10.1200/jco.2008.14.0095.

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Purpose To compare three-drug chemotherapy with cisplatin, doxorubicin, and methotrexate with four-drug chemotherapy with cisplatin, doxorubicin, methotrexate, and ifosfamide for the treatment of osteosarcoma. To determine whether the addition of muramyl tripeptide (MTP) to chemotherapy enhances event-free survival (EFS) and overall survival in newly diagnosed patients with osteosarcoma. Patients and Methods Six hundred sixty-two patients with osteosarcoma without clinically detectable metastatic disease and whose disease was considered resectable received one of four prospectively randomized treatments. All patients received identical cumulative doses of cisplatin, doxorubicin, and methotrexate and underwent definitive surgical resection of primary tumor. Patients were randomly assigned to receive or not to receive ifosfamide and/or MTP in a 2 × 2 factorial design. The primary end points for analysis were EFS and overall survival. Results In the current analysis, there was no evidence of interaction, and we were able to examine each intervention separately. The chemotherapy regimens resulted in similar EFS and overall survival. There was a trend toward better EFS with the addition of MTP (P = .08). The addition of MTP to chemotherapy improved 6-year overall survival from 70% to 78% (P = .03). The hazard ratio for overall survival with the addition of MTP was 0.71 (95% CI, 0.52 to 0.96). Conclusion The addition of ifosfamide to cisplatin, doxorubicin, and methotrexate did not enhance EFS or overall survival for patients with osteosarcoma. The addition of MTP to chemotherapy resulted in a statistically significant improvement in overall survival and a trend toward better EFS.
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Gangemi, J. D., M. Nachtigal, D. Barnhart, L. Krech, and P. Jani. "Therapeutic Efficacy of Liposome-Encapsulated Ribavirin and Muramyl Tripeptide in Experimental Infection with Influenza or Herpes Simplex Virus." Journal of Infectious Diseases 155, no. 3 (March 1, 1987): 510–17. http://dx.doi.org/10.1093/infdis/155.3.510.

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48

Guan, Rongjin, Abhijit Roychowdury, Brian Ember, Sanjay Kumar, Geert-Jan Boons, and Roy A. Mariuzza. "Crystal structure of a peptidoglycan recognition protein (PGRP) in complex with a muramyl tripeptide from Gram-positive bacteria." Journal of Endotoxin Research 11, no. 1 (February 1, 2005): 41–46. http://dx.doi.org/10.1179/096805105225006713.

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Guan, Rongjin, Abhijit Roychowdury, Brian Ember, Sanjay Kumar, Geert-Jan Boons, and Roy A. Mariuzza. "Crystal structure of a peptidoglycan recognition protein (PGRP) in complex with a muramyl tripeptide from Gram-positive bacteria." Journal of Endotoxin Research 11, no. 1 (February 2005): 41–46. http://dx.doi.org/10.1177/09680519050110010901.

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Fujimaki, Wakae, Kyogo Itoh, Taeha An, Jacalyn B. Gano, Merrick I. Ross, Paul F. Mansfield, Charles M. Balch, et al. "Cytokine Production and Immune Cell Activation in Melanoma Patients Treated with Liposomal Muramyl Tripeptide (CGP 19835A Lipid)1." Cancer Biotherapy 8, no. 4 (January 1993): 307–18. http://dx.doi.org/10.1089/cbr.1993.8.307.

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