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Mini-Reviews in Medicinal Chemistry, Volume 3, No. 3, 2003

 

Contents

 

Peptide Derivatives as Agonists or Antagonists of Formylpeptide Receptors: Analysis of their Effects on Neutrophils Pp.167-173

Alessandro Dalpiaz  and Angelo Scatturin

[Abstract]

 

Biological Role of Formaldehyde, and Cycles Related to Methylation, Demethylation, and Formaldehyde Production Pp.175-192

Huba Kalasz

[Abstract]

 

Vitamin D Receptor as a Drug Discovery Target Pp.193-204

Karen V. Pinette , Ying K. Yee , Bernard Y. Amegadzie  and Sunil Nagpal

[Abstract]

 

New Aspects of Cyclosporin A Mode of Action: from Gene Silencing to Gene Up-Regulation Pp.205-214

Laurent Mascarell and Paolo Truffa-Bachi

[Abstract]

 

The 1,4-Dihydropyridine Nucleus: A Pharmacophoric Template Part 1. Actions at Ion Channels Pp.215-223

David J. Triggle

[Abstract]

 

Steroid 5a-Reductase Inhibitors Pp.225-237

Eugenio Flores, Eugene Bratoeff , Marisa Cabeza , Elena Ramirez, Alexandra Quiroz and Ivonne Heuze

[Abstract]

 

Current Strategies for the Development of Novel Antipsychotic Drugs Pp.239-251

Jordi Bolos

[Abstract]

 

Biological Properties and Therapeutic Potential of Bilirubin Pp.253-256

Ross P. McGeary , Alexander J. Szyczew  and Istvan Toth

[Abstract]

 

The p53-Mdm2 Pathway: Targets for the Development of New Anticancer Therapeutics Pp.257-270

Daniella I. Zheleva, David P. Lane and Peter M. Fischer

[Abstract]

 

Abstracts

 

[Back to top] Peptide Derivatives as Agonists or Antagonists of Formylpeptide Receptors: Analysis of their Effects on Neutrophils

Alessandro Dalpiaz  and Angelo Scatturin

 

The effects of peptide derivatives as agonists or antagonists of formylpeptide receptors are described, taking into account the related cellular responses by neutrophils. These effects are related to the structure of peptide derivatives, some of which are potent anti HIV-1 agents. Finally, formylpeptide receptor models are depicted.

 

[Back to top] Biological Role of Formaldehyde, and Cycles Related to Methylation, Demethylation, and Formaldehyde Production

Huba Kalasz

 

An overview is given on the analysis, formation, role and occurrence of formaldehyde in living organisms.

 

Various methods have been used for the determination of formaldehyde in tissues and body fluids. Gas chromatography, thin-layer chromatography and HPLC were employed for the analysis of formaldehyde, mainly after derivatization. The formaldehyde level of human blood and urine was found at the low ppm level. The formaldehyde level could be increased upto several ten mg/mL-1 following special dietary supply.

 

Biochemical pathway of both the formaldehyde production and demethylation/methylation processes is generally connected to the methionine – homocysteine cycles. Another important way of demethylation generated formaldehyde production is given by microsomal cytochrome P-450 dependent oxidation of xenobiotics, such as various drugs prescribed by doctors. Semicarbazide sensitive amine oxidase also produces formaldehyde.

 

Increased level of formaldehyde may be the indication of either patho-physiological processes, or environmental contamination, or malnutrition.

 

The formaldehyde-related methylation and demethylation procedures are also detailed. DNA methylation may have an important role in the pathogenesis of certain diseases.

 

[Back to top] Vitamin D Receptor as a Drug Discovery Target

Karen V. Pinette , Ying K. Yee , Bernard Y. Amegadzie  and Sunil Nagpal

 

1a, 25-dihydroxyvitamin D3 [1,25 (OH)2D3], the active metabolite of vitamin D3, is known for the maintenance of normal skeleton architecture and mineral homeostasis. Apart form these traditional calcemic actions, 1,25 (OH)2D3 and its synthetic analogs are increasingly recognized for their potent anti-proliferative, prodifferentiative and immunomodulatory activities. The calcemic and non-calcemic actions of 1,25 (OH)2D3 and its synthetic analogs are mediated through vitamin D receptor (VDR), which belongs to the superfamily of steroid/thyroid hormone nuclear receptors. Physiological and pharmacological actions of 1,25 (OH)2D3 in various systems, along with the detection of VDR in target cells, have indicated potential applications of VDR ligands in inflammation, dermatological indications, osteoporosis, cancers and autoimmune diseases. VDR ligands have shown therapeutic potential in limited clinical trials as well as in animal models of these diseases. As a result, a VDR ligand, calcipotriol is in clinic for psoriasis and another, OCT, [2-oxa-1,25 (OH)2D3] is being developed as a topical agent for the same indication. Further, 1a,-hydroxyvitamin D3 (alphacalcidol), a prodrug of 1,25 (OH)2D3 is in clinic and a synthetic VDR ligand, ED-71, is under consideration for approval in Japan for the treatment of osteoporosis. Interestingly, VDR ligands have shown not only preventive but also potent therapeutic anabolic activities in animal models of osteoporosis. However, the wide spread use of VDR ligands in above-mentioned indications is hampered by their major side effect, namely hypercalcemia. In view of this associated toxicity, synthetic VDR ligands with reduced calcemic potential have been synthesized with the ultimate aim of improving their therapeutic efficacy. This review presents recent advances in VDR biology, novel VDR ligands and therapeutic applications of VDR ligands.

 

[Back to top] New Aspects of Cyclosporin A Mode of Action: from Gene Silencing to Gene Up-Regulation

Laurent Mascarell and Paolo Truffa-Bachi

 

Cyclosporin A (CSA) has transformed clinical transplantation, both in term of success and of quality-of-life of the patient. Studies aimed to unfold the site of CSA action have shown that this molecule binds to cytosolic proteins of the cyclophilin family. CSA:cyclophilin complexes have a high affinity for calcineurin, a key enzyme in T-cell activation. By blocking the calcineurin activity, CSA prevents the induction of genes encoding for cytokines and their receptors. Thus, humoral and cellular immune responses are abolished, this resulting in the successful graft acceptance. Disappointingly, CSA and the other molecules as FK506, sharing the capacity to inhibit calcineurin, should be administered for all patient life, as tolerance to alloantigens is not achieved by these molecules. The long term utilization of this class of immunosuppressors increases the incidence of different tumors. The finding that CSA does not interfere with various biochemical pathways has prompted different groups to analyze a possible effect of CSA on molecules that might be involved in different functions of the immune response and/or in tumorogenesis. A new picture of CSA mode of action is emerging in which the immunosuppressor prevents the transcription of a group of genes, concomitantly inducing the transcription of another set. Here, we review the data and discuss the consequences of these new findings in term of T-cell activation mechanisms.

 

[Back to top] The 1,4-Dihydropyridine Nucleus: A Pharmacophoric Template Part 1. Actions at Ion Channels

David J. Triggle

 

The 1,4-dihydropyridine nifedipine is a prototypical example of the group of calcium channel blockers that also includes a number of second and third generation agents. These drugs enjoy substantial therapeutic prominence for their cardiovascular actions, including hypertension and angina. These actions are exerted at a specific member of the voltage-gated calcium channel family –the L-type channel. However, it is increasingly clear that the 1,4-dihydropyridine structure is a pharmacophoric template or “privileged structure” that, when appropriately substituted, can exert potent and selective actions at a diverse set of membrane receptors, including ion channels, G protein-coupled receptors and enzymes. This review will summarize the actions of 1,4-dihydropyridines at these receptors and advance the case that the 4-phenyl-1,4- dihydropyridine structure is a particularly versatile drug template. Part I of the review will summarize actions at ion channels and part II will summarize actions at other receptor systems.

 

[Back to top] Steroid 5a-Reductase Inhibitors

Eugenio Flores, Eugene Bratoeff , Marisa Cabeza , Elena Ramirez, Alexandra Quiroz and Ivonne Heuze

 

The objective of this study is to synthesize new steroidal compounds based on the progesterone skeleton with a high inhibitory activity for the enzyme 5a-reductase. Presently similar compounds are being used for the treatment of androgen dependent diseases such as: hirsutism, androgenic alopecia, bening prostatic hyperplasia and prostate cancer. Dihydrotestosterone 2 (Fig. (1)), a 5a-reduced metabolite of testosterone 1 has been implicated as a causative factor in the progression of these diseases, largely through the clinical evaluation of males who are genetically deficient of steroid 5a-reductase enzyme. As a result of this study, the inhibition of this enzyme has become a pharmacological strategy for the design and synthesis of new antiandrogenic drugs. The advent of finasteride 8 (Fig. (4)) a 5a-reductase inhibitor has grately alleviated the symptoms associated with benign prostatic hyperplasia.

 

In our laboratory we recently synthesized several new 16b-methyl-pregnadiene-3,20-diones derivatives 27 (Fig.(6)), 38-42 (Fig. (11)), 16b-phenyl-pregnadiene-3,17a-dione derivatives 32-33 (Fig. (7)), 16b-phenylpregnatriene- 3,17a-diones, 30, 31 (Fig. (7)) and 16b-methyl-pregnatriene-3,20-diones 43-46 (Fig. (11)). These compounds were evaluated as 5a-reductase inhibitors in the following biological models: Penicillium crustosum broths, the flank organs of gonadectomized male hamsters, the incorporation of radiolabeled sodium acetate into lipids, the effect of the new steroids on the reduction of the weight of the seminal vesicles and on the in vitro metabolism of [3H]T to [3H]DHT in seminal vesicles homogenates of gonadectomized male hamsters. All trienones 30, 31, and 43-46 in all biological models showed consistently a higher 5a-reductase inhibitory activity than the corresponding dienones 27, 32, 33 and 38-42. We believe that with these compounds the 5a-reductase enzyme is inactivated by an irreversible Michael type addition of the nucleophilic portion of the enzyme to the conjugated double bond of the steroid. The trienones having a more coplanar structure react faster with the enzyme and thus show a higher inhibitory activity.

 

[Back to top] Current Strategies for the Development of Novel Antipsychotic Drugs

Jordi Bolos

 

While classical neuroleptics are characterized by dopamine D2 antagonism, this is also considered to be the cause of their neurological side effects. In recent years, novel antipsychotic drugs with improved efficacy, devoid of extrapyramidal effects are being developed. The mechanisms of action of these new atypical antipsychotics can be classified into three general groups: a) binding to D2 together with non-dopaminergic receptors, b) interaction with dopamine receptor subtypes other than D2 and c) selective binding to nondopaminergic systems, such as glutamatergic, sigma, neurotensin, and cannabinoid.

 

[Back to top] Biological Properties and Therapeutic Potential of Bilirubin

Ross P. McGeary , Alexander J. Szyczew  and Istvan Toth

 

Bilirubin was long considered a useless metabolite of heme catabolism, responsible for the clinical manifestation of jaundice, and potentially toxic in high doses, particularly in neonates. In the past two decades the potent biological properties of bilirubin, particularly as an antioxidant, have been recognised, and this has prompted a number of investigations into this molecule concerning its in vitro and in vivo properties. This review summarises that work, as well as more recent investigations into the potential therapeutic uses of bilirubin.

 

[Back to top] The p53-Mdm2 Pathway: Targets for the Development of New Anticancer Therapeutics

Daniella I. Zheleva, David P. Lane and Peter M. Fischer

 

The tumour suppressor p53 is at the centre of a network of regulatory pathways that guard over the continued integrity of the living cell and its progeny after exposure to different forms of stress, particularly those capable of inducing DNA damage. Tumour cells very frequently circumvent this control by disabling the function of p53, or other proteins in the p53 network, through mutation. Here we review the different therapeutic strategies that have been adopted to exploit common neoplastic aberrations in the p53 pathways. We emphasise in particular those approaches where modulation with pharmaceutical agents has already shown some promise, including pharmacological rescue of mutant p53, modulation of the protein-protein interaction between p53 and one of its negative regulators, Mdm2, as well as interference with downstream targets.