Arbaprostil (15(R)-15-methylprostaglandin E2) is a prodrug, which is activated by epimerization to form the active S-epimer. It was shown, that arbaprostil markedly accelerated the healing rate of active duodenal ulcers, due to inhibition of acid secretion as well as gastric cytoprotection.

Desfesoterodine is an active metabolite of antimuscarinic drugs for the treatment of overactive bladder fesoterodine and tolterodine. In contrast to the cytochrome P450 (CYP) 2D6-mediated metabolism of tolterodine, desfesoterodine formation from fesoterodine occurs via ubiquitous nonspecific esterases. Serum levels of the desfesoterodine in humans are generally comparable to those of tolterodine following oral administration of the parent compound. The pharmacological in vitro and in vivo profiles of desfesoterodine are almost identical to those of tolterodin. The potent antimuscarinic action of desfesoterodine on the urinary bladder was confirmed in the in vivo studies and, like tolterodine, desfesoterodine was significantly more potent in inhibiting bladder contractions than salivation in the anaesthetised cat. Desfesoterodine is more potent than tolterodine in vivo. The apparent difference in potency in vivo might be explained by the degree of serum protein binding of the two compounds. The fraction of unbound drug in serum is larger for desfesoterodine than for tolterodine. Desfesoterodine may contribute to the therapeutical action of tolterodine.

Desfesoterodine is an active metabolite of antimuscarinic drugs for the treatment of overactive bladder fesoterodine and tolterodine. In contrast to the cytochrome P450 (CYP) 2D6-mediated metabolism of tolterodine, desfesoterodine formation from fesoterodine occurs via ubiquitous nonspecific esterases. Serum levels of the desfesoterodine in humans are generally comparable to those of tolterodine following oral administration of the parent compound. The pharmacological in vitro and in vivo profiles of desfesoterodine are almost identical to those of tolterodin. The potent antimuscarinic action of desfesoterodine on the urinary bladder was confirmed in the in vivo studies and, like tolterodine, desfesoterodine was significantly more potent in inhibiting bladder contractions than salivation in the anaesthetised cat. Desfesoterodine is more potent than tolterodine in vivo. The apparent difference in potency in vivo might be explained by the degree of serum protein binding of the two compounds. The fraction of unbound drug in serum is larger for desfesoterodine than for tolterodine. Desfesoterodine may contribute to the therapeutical action of tolterodine.

Desfesoterodine is an active metabolite of antimuscarinic drugs for the treatment of overactive bladder fesoterodine and tolterodine. In contrast to the cytochrome P450 (CYP) 2D6-mediated metabolism of tolterodine, desfesoterodine formation from fesoterodine occurs via ubiquitous nonspecific esterases. Serum levels of the desfesoterodine in humans are generally comparable to those of tolterodine following oral administration of the parent compound. The pharmacological in vitro and in vivo profiles of desfesoterodine are almost identical to those of tolterodin. The potent antimuscarinic action of desfesoterodine on the urinary bladder was confirmed in the in vivo studies and, like tolterodine, desfesoterodine was significantly more potent in inhibiting bladder contractions than salivation in the anaesthetised cat. Desfesoterodine is more potent than tolterodine in vivo. The apparent difference in potency in vivo might be explained by the degree of serum protein binding of the two compounds. The fraction of unbound drug in serum is larger for desfesoterodine than for tolterodine. Desfesoterodine may contribute to the therapeutical action of tolterodine.

Desfesoterodine is an active metabolite of antimuscarinic drugs for the treatment of overactive bladder fesoterodine and tolterodine. In contrast to the cytochrome P450 (CYP) 2D6-mediated metabolism of tolterodine, desfesoterodine formation from fesoterodine occurs via ubiquitous nonspecific esterases. Serum levels of the desfesoterodine in humans are generally comparable to those of tolterodine following oral administration of the parent compound. The pharmacological in vitro and in vivo profiles of desfesoterodine are almost identical to those of tolterodin. The potent antimuscarinic action of desfesoterodine on the urinary bladder was confirmed in the in vivo studies and, like tolterodine, desfesoterodine was significantly more potent in inhibiting bladder contractions than salivation in the anaesthetised cat. Desfesoterodine is more potent than tolterodine in vivo. The apparent difference in potency in vivo might be explained by the degree of serum protein binding of the two compounds. The fraction of unbound drug in serum is larger for desfesoterodine than for tolterodine. Desfesoterodine may contribute to the therapeutical action of tolterodine.

Ormaplatin (NSC 363812, tetraplatin) is a stable platinum (IV) analog. Ormaplatin alkylates DNA, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity. Ormaplatin showed marked antitumor activity both in vitro and vivo. The severe, cumulative and irreversible peripheral neurotoxicity observed in phase I studies resulted in termination of further clinical development of ormaplatin.

Ormaplatin (NSC 363812, tetraplatin) is a stable platinum (IV) analog. Ormaplatin alkylates DNA, forming both inter- and intra-strand platinum-DNA crosslinks, which result in inhibition of DNA replication and transcription and cell-cycle nonspecific cytotoxicity. Ormaplatin showed marked antitumor activity both in vitro and vivo. The severe, cumulative and irreversible peripheral neurotoxicity observed in phase I studies resulted in termination of further clinical development of ormaplatin.

Sonepiprazole exhibits highly specific binding to the D4 dopamine receptor with more than 100-fold selectivity for the D4 receptor over other receptors, including dopamine, serotonin, and adrenergic receptors. It is a neutral antagonist at the D4 dopamine receptor and is devoid of dopamine agonist activity. Sonepiprazole selectively induces c-fos expression in the prefrontal cortex and blocks behavioral, biochemical, and genomic effects of repeated amphetamine administration in rats. Sonepiprazole was investigated as an antipsychotic for the treatment of schizophrenia in a placebo-controlled clinical trial, but in contrast to its comparator olanzapine no benefits were found and it was not researched further for this indication.

Piriprost (U-60, 257) is a structural analog of prostaglandin I2 (PGI2) with low IP receptor-mediated activity. It inhibits 5-LO (5-lipoxygenase). Piriprost inhibits the release of histamine and leukotrienes, implicating its role in inflammation and allergic responses. However, it was shown, that piriprost did not influence the airway responses after allergen in asthma. Nevertheless, even more, the drug was irritant to the respiratory tract than was placebo.

Ritipenem (FCE 22101), a penem antibiotic, penicillin binding protein inhibitor, is potent against both gram-positive and -negative bacteria, and its acetoxymethyl ester (FCE 22891; ritipenem-acoxil) is orally available. Ritipenem is manufactured by Tanabe Seiyaku in the ritipenem acoxil prodrug form, which can be taken orally. It is not FDA approved in the United States.