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Thalidomide and its Analogs: A Potential Immunomodulatory Alternative for Treating Liver Diseases and Cirrhosis, pp. 33-62 $100.00
Authors:  (Eduardo Fernández-Martínez, Laboratory of Medicinal Chemistry and Pharmacology, Área Académica de Medicina del Instituto de Ciencias de la Salud (I.C.Sa.), Universidad Autónoma del Estado de Hidalgo (UAEH), México)
Thalidomide is currently used for treating erythema nodosum leprosum, multiple
myeloma, angiogenesis, rheumatoid arthritis, graft-versus-host disease, among others.
Thalidomide effects are related to its capacity to inhibit the proinflammatory cytokine
tumor necrosis factor-α (TNF-α) and, in consequence, causes immunomodulation on
other cytokines. During the establishment of some diseases the balance between
proinflammatory and antiinflammatory cytokines is disrupted, promoting a pathological
state; thus, elevated levels of proinflammatory cytokines mediate several deleterious
processes such as inflammation, necrosis, apoptosis and fibrosis. These events are
present in acute and chronic degenerative liver diseases such as hepatitis, cholangitis,
cirrhosis and hepatocellular carcinoma (HCC). Then, the immunomodulation on
cytokines by drugs seems to be a pharmacological target to ameliorate liver damage and
cirrhosis. In fact, there are not sufficient drugs for relief or cure of cirrhosis currently;
some of these few are expensive, unstable and palliative or may cause side effects. Novel
thalidomide analogs have been synthesized with improved stability and potency as TNF-
α inhibitory and immunomodulatory agents, besides low or none teratogenicity.
Experimental assessment of thalidomide and its analogs in animal models of liver injury
have afforded very hopeful outcomes. Thalidomide and two analogs have evidenced
anticholestatic, antinecrotic and antifibrotic activities in bile duct ligation-induced biliary
cirrhosis. Another analog protected D-galactosamine/endotoxin-treated mice from liver
damage. Thalidomide ameliorated the alcoholic hepatic injury and prevented necrosis,
cholestasis and fibrosis induced by CCl4 in rats. Moreover, this drug salvaged from lethal
hepatic necroinflammation and accelerated the recovery from established thioacetamideprovoked
cirrhosis in rats. The antiinflammatory, antinecrotic and antifibrotic effects
elicited by thalidomide and its analogs are mainly mediated by the inhibition on TNFthrough
two different routes, as well as the down-regulation of nuclear factor- B (NFB)
signaling pathway and by diminishing adhesion molecules to prevent the progression
of liver fibrosis and cirrhosis. Furthermore, thalidomide showed beneficial effects on
HCC by decreasing angiogenesis and metastasis in murine models; therefore, diverse
clinical phase I/II studies were carried out to evaluate its antitumoral or disease control
outcomes. However, thalidomide as a single drug therapy yields very modest benefits,
although in most cases this is well tolerated and offers disease stabilization. Different
doses and the combination with other chemotherapeutic agents appear to enhance
therapeutic effects; the assessment of the new thalidomide analogs in next clinical trials
of HCC healing is strongly suggested. Thalidomide and its analogs may be a feasible
option for the treatment of liver diseases and cirrhosis. 

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Thalidomide and its Analogs: A Potential Immunomodulatory Alternative for Treating Liver Diseases and Cirrhosis, pp. 33-62