Genomic signaling
Genomic mechanisms, regardless of which type, elicit responses with a slow onset and a slow dissipation. This is attributed to the duration of mRNA transcription and translation. Glucocorticoids have the ability to regulate roughly 100 to 1000 genes with specificity to cell-type.Three major mechanisms have described how the MP-GR complex alter gene expression by either binding to DNA or transcription modulators. One mechanism of genomic signaling occurs when the MP-GR complex directly binds to DNA sequences called glucocorticoid response elements (GREs). GREs are located in regulatory regions of target genes and mediate their transactivation or transrepression. For example, the activation of lipocortin 1 (ANAX1) negatively interferes with the production of prostaglandins and leukotrienes, known pro-inflammatory signals. Likewise, negative GREs (nGREs) are responsible for repressing genes involved in immune cell activation. Post transcriptional  modifications
Post translational modifications (PTMs) also contribute to methylprednisolone signaling and can produce genomic and non-genomic effects. The GR has contains several sites for phosphorylation, sumoylation, ubiquitination, and acetylation that primarily occurs after intracellular methylprednisolone binding to the GR. PTMs modulate many functions including nuclear translocation, strength and duration of receptor signaling and cofactor interaction. A specific example is the deacetylation by histone deacetylase 2 (HDACe) was necessary for transrepression of  NF-κB. Non-genomic signaling
The mechanisms of non-genomic signaling are distinct from genomic signaling, yet mediate similar pathways and provide therapeutic relevance.
The racemization process can occur in vivo. The process of conversion of one enantiomer to its mirror-image version with no other change in the molecule is called chiral inversion.Celgene Corporation originally synthesized thalidomide using a three-step sequence starting with L-glutamic acid treatment, but this has since been reformed by the use of L-glutamine. As shown in the image below, N-carbethoxyphthalimide (1) can react with L-glutamine to yield N-phthaloyl-L-glutamine (2). Cyclization of N-phthaloyl-L-glutamine occurs using carbonyldiimidazole, which then yields thalidomide (3). Celgene Corporations original method resulted in a 31% yield of S-thalidomide, whereas the two-step synthesis yields 85–93% product that is 99% pure. History
In 1952, thalidomide was synthesised by Chemical Industry Basel (CIBA), but was found "to have no effect on animals and was discarded" on that basis. In 1957, it was acquired by Chemie Grünenthal in Germany. The German company had been established as a soap maker after World War II ended, to address the urgent market need for antibiotics. Heinrich Mückter was appointed to head the discovery program based on his experience working with the German armys antiviral research. While preparing reagents for the work, Mueckters assistant Wilhelm Kunz isolated a by-product that was recognized by pharmacologist Herbert Keller as an analog of glutethimide, a sedative. The medicinal chemistry work turned to improving the lead compound into a suitable drug: the result was thalidomide.