Ritalinic acid is an inactive, major metabolite of methylphenidate, a schedule II drug in the United States commonly used as a psychostimulant drugs methylphenidate and ethylphenidate. The elimination half-life of methylphenidate is relatively short (approximately 2 hours); therefore it is also available in extended release (ER) forms. The main metabolite is ritalinic acid, and the methylphenidate metabolites are mostly excreted in urine.

Dihydro-β-erythroidine is a competitive nicotinic acetylcholine receptor antagonist with moderate selectivity for the neuronal α4 receptor subunit. Dihydro-β-erythroidine have curare-like effects at peripheral nicotinic receptors, which include severe respiratory depression. Thus in vivo behavioral studies using Dihydro-β-erythroidine are limited. Dihydro-β-erythroidine antagonizes behavioral effects of nicotine in vivo. After s.c. administration, Dihydro-β-erythroidine was potent in blocking nicotine's effects except for antinociception. Intrathecal injection of Dihydro-β-erythroidine was effective in blocking the antinociceptive effect of nicotine.

Pelletierine +/- also known as isopelletierine is an alkaloid found in the root-bark of the pomegranate tree. There is a little information about the pharmacological application of this compound, but one article describes its anthelminthic activity.

Perfluorooctane sulfonic acid (PFOS) is a global pollutant and an environmental toxicant, widely used as a fabric protector, serving as a stain repellant in drapery, carpets, and clothing. While its use in Europe, Canada, and the U.S. has been banned due to its human toxicity, it continues to be used in China and other developing countries as a global pollutant. However, epidemiologic evidence does not support a causal association between PFOS exposure and cancer risk in humans. However, in utero exposure to PFOS adversely affect the fetal synthesis and secretion of reproductive hormones (e.g., testosterone, estradiol, and inhibin B) in humans. Since the half-life of PFOS is relatively long, at 5.4-yr, even low-dose exposure to PFOS can accumulate in the body over an extended period of time. The mechanisms of PFOA -induced hepatic dysfunction are not completely understood but was shown, that PFOS induces their effects via targeting hepatocyte nuclear factor 4-alpha (HNF4α) and thus altered its conformation. In addition, some recent experiments in vitro revealed, that PFOS-induced male reproductive dysfunction can possibly be managed through an intervention on Akt1/2 expression.

Naftopidil,(R)- is an enantiomer of Naftopidil (NAF), a specific subtype selective α1-adrenoceptor blocker. Racemic Naftopidil is frequently used for the treatment of lower urinary tract symptoms/benign prostatic hyperplasia. No significant differences in pharmacokinetic parameters were observed between R(+)- and S(−)-NAF after intravenous administration. However, mean plasma concentrations of S(−)-NAF were higher than those of R(+)-NAF after intragastric administration. S(−)-NAF reached higher plasma concentrations within shorter times and achieved lower plasma CL within 24 h than R(+)-NAF. S(−)-NAF bioavailability in rats was consistently about two-fold higher than that of R(+)-NAF. The major pathways of S(−)-NAF metabolism in vitro were demethylation and hydroxylation. CYP2C9 played the most important role in the demethylation and hydroxylation of both NAF enantiomers.

Naftopidil,(R)- is an enantiomer of Naftopidil (NAF), a specific subtype selective α1-adrenoceptor blocker. Racemic Naftopidil is frequently used for the treatment of lower urinary tract symptoms/benign prostatic hyperplasia. No significant differences in pharmacokinetic parameters were observed between R(+)- and S(−)-NAF after intravenous administration. However, mean plasma concentrations of R(+)-NAF were lower than those of S(-)-NAF after intragastric administration. R(+)-NAF bioavailability in rats was consistently about two-fold lower than that of S(-)-NAF. The fractions of R(+)- NAF reaching the prostate and metabolized in the liver were higher than those of S(−)-NAF. The major pathways of R(+)- NAF metabolism in vitro were demethylation and hydroxylation. CYP2C9 played the most important role in the demethylation and hydroxylation of both NAF enantiomers. CYP2C19 was another CYP isoform that played a major role in R(+)-NAF metabolism.

1-(2-Chloroethyl)pyrrolidine is a haloalkyl substituted pyrrolidine. It is an intermediate in the synthesis of various pharmaceutical compound. For example, 1-(2-Chloroethyl)pyrrolidine is used for the synthesis of cholinesterase inhibitors and nonsteroidal selective estrogen receptor modulator nafoxidine.

A copper fungicide.

Alfuzosin, a quinazoline derivative, acts as a selective and competitive antagonist of alpha 1-adrenoceptor-mediated contraction of prostatic, prostatic capsule, bladder base and proximal urethral smooth muscle, thereby reducing the tone of these structures. Consequently, urethral pressure and resistance, bladder outlet resistance, bladder instability and symptoms associated with benign prostatic hyperplasia are reduced. The two enantiomers (S and R) have the same pharmacological activity as the racemate. Ligand binding and functional studies demonstrate that the alpha1-antagonist properties of alfuzosin reside equally in its two enantiomers. Racemic alfuzosin is indicated for the symptomatic treatment of benign prostatic hyperplasia and adjunctive therapy in acute urinary retention.

Alfuzosin, a quinazoline derivative, acts as a selective and competitive antagonist of alpha 1-adrenoceptor-mediated contraction of prostatic, prostatic capsule, bladder base and proximal urethral smooth muscle, thereby reducing the tone of these structures. Consequently, urethral pressure and resistance, bladder outlet resistance, bladder instability and symptoms associated with benign prostatic hyperplasia are reduced. The two enantiomers (S and R) have the same pharmacological activity as the racemate. Ligand binding and functional studies demonstrate that the alpha1-antagonist properties of alfuzosin reside equally in its two enantiomers. Racemic alfuzosin is indicated for the symptomatic treatment of benign prostatic hyperplasia and adjunctive therapy in acute urinary retention.