Fmoc-alpha-Me-L-Cys(Mmt)-OH
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Fmoc-alpha-Me-L-Cys(Mmt)-OH

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Category
Fmoc-Amino Acids
Catalog number
BAT-008213
CAS number
1198791-74-0
Molecular Formula
C39H35NO5S
Molecular Weight
629.8
IUPAC Name
(2R)-2-(9H-fluoren-9-ylmethoxycarbonylamino)-3-[(4-methoxyphenyl)-diphenylmethyl]sulfanyl-2-methylpropanoic acid
Synonyms
(R)-L-N-Fmoc-S-Mmt-a-Methylcysteine
Storage
Store at 2-8°C
InChI
InChI=1S/C39H35NO5S/c1-38(36(41)42,40-37(43)45-25-35-33-19-11-9-17-31(33)32-18-10-12-20-34(32)35)26-46-39(27-13-5-3-6-14-27,28-15-7-4-8-16-28)29-21-23-30(44-2)24-22-29/h3-24,35H,25-26H2,1-2H3,(H,40,43)(H,41,42)/t38-/m0/s1
InChI Key
FTIUQZHUKYUVEE-LHEWISCISA-N
Canonical SMILES
CC(CSC(C1=CC=CC=C1)(C2=CC=CC=C2)C3=CC=C(C=C3)OC)(C(=O)O)NC(=O)OCC4C5=CC=CC=C5C6=CC=CC=C46
1. Multiple cell types contribute to the atherosclerotic lesion fibrous cap by PDGFRβ and bioenergetic mechanisms
Alexandra A C Newman, et al. Nat Metab. 2021 Feb;3(2):166-181. doi: 10.1038/s42255-020-00338-8. Epub 2021 Feb 22.
Stable atherosclerotic plaques are characterized by a thick, extracellular matrix-rich fibrous cap populated by protective ACTA2+ myofibroblast (MF)-like cells, assumed to be almost exclusively derived from smooth muscle cells (SMCs). Herein, we show that in murine and human lesions, 20% to 40% of ACTA2+ fibrous cap cells, respectively, are derived from non-SMC sources, including endothelial cells (ECs) or macrophages that have undergone an endothelial-to-mesenchymal transition (EndoMT) or a macrophage-to-mesenchymal transition (MMT). In addition, we show that SMC-specific knockout of the Pdgfrb gene, which encodes platelet-derived growth factor receptor beta (PDGFRβ), in Apoe-/- mice fed a Western diet for 18 weeks resulted in brachiocephalic artery lesions nearly devoid of SMCs but with no changes in lesion size, remodelling or indices of stability, including the percentage of ACTA2+ fibrous cap cells. However, prolonged Western diet feeding of SMC Pdgfrb-knockout mice resulted in reduced indices of stability, indicating that EndoMT- and MMT-derived MFs cannot compensate indefinitely for loss of SMC-derived MFs. Using single-cell and bulk RNA-sequencing analyses of the brachiocephalic artery region and in vitro models, we provide evidence that SMC-to-MF transitions are induced by PDGF and transforming growth factor-β and dependent on aerobic glycolysis, while EndoMT is induced by interleukin-1β and transforming growth factor-β. Together, we provide evidence that the ACTA2+ fibrous cap originates from a tapestry of cell types, which transition to an MF-like state through distinct signalling pathways that are either dependent on or associated with extensive metabolic reprogramming.
2. Tecemotide: an antigen-specific cancer immunotherapy
Gregory T Wurz, Chiao-Jung Kao, Michael Wolf, Michael W DeGregorio Hum Vaccin Immunother. 2014;10(11):3383-93. doi: 10.4161/hv.29836.
The identification of tumor-associated antigens (TAA) has made possible the development of antigen-specific cancer immunotherapies such as tecemotide. One of those is mucin 1 (MUC1), a cell membrane glycoprotein expressed on some epithelial tissues such as breast and lung. In cancer, MUC1 becomes overexpressed and aberrantly glycosylated, exposing the immunogenic tandem repeat units in the extracellular domain of MUC1. Designed to target tumor associated MUC1, tecemotide is being evaluated in Phase III clinical trials for treatment of unresectable stage IIIA/IIIB non-small cell lung cancer (NSCLC) as maintenance therapy following chemoradiotherapy. Additional Phase II studies in other indications are ongoing. This review discusses the preclinical and clinical development of tecemotide, ongoing preclinical studies of tecemotide in human MUC1 transgenic mouse models of breast and lung cancer, and the potential application of these models for optimizing the timing of chemoradiotherapy and tecemotide immunotherapy to achieve the best treatment outcome for patients.
3. Synthesis of the very acid-sensitive Fmoc-Cys(Mmt)-OH and its application in solid-phase peptide synthesis
K Barlos, D Gatos, O Hatzi, N Koch, S Koutsogianni Int J Pept Protein Res. 1996 Mar;47(3):148-53. doi: 10.1111/j.1399-3011.1996.tb01338.x.
S-4-methoxytrityl cysteine was synthesized and converted into the corresponding Fmoc-Cys(Mmt)-OH by its reaction with Fmoc-OSu. As compared to the corresponding Fmoc-Cys(Trt)-OH, the S-Mmt-function was found to be considerably more acid labile. Quantitative S-Mmt-removal occurs selectively in the presence of groups of the tert butyl type and S-Trt by treatment with 0.5-1.0% TFA. The new derivative was successfully utilized in the SPPS of Tyr1-somatostatin on 2-chlorotrityl resin. In this synthesis groups of the Trt-type were exclusively used for amino acid side-chain protection. Quantitative cleavage from the resin and complete deprotection was performed by treatment with 3% TFA in DCM-TES (95:5) for 30 min at RT. We observed no reduction of tryptophan under these conditions.
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