Quinoline Hydrochloride Research Articles

Effects of dopaminergic agents on carrageenan hyperalgesia after intrathecal administration to rats

The present study explored the role of dopaminergic transmission in spinal cord in a model of carrageenan-induced inflammatory pain by examining the effects of selective agonists and antagonists of dopamine receptors. The results were as follows: (1) trans-(−)-4 aR-4,4 a,5,6,7,8,8 a,9-octahydro-5-propyl-1 H-pyrazolo[3,4− g] quinoline hydrochloride (LY171555), a dopamine D 2 receptor agonist, produced anti-hyperalgesia (150 and 300 nmol) or hypoalgesia (300 nmol) in the inflamed hindpaws and non-inflamed hindpaws, respectively; spiperone hydrochloride (8-[4-(4-fluorophenyl)-4-oxobutyl]-1-phenyl-1,3,8-triazaspiro[4,5]decan-4-one hydrochloride), a dopamine D 2 receptor antagonist, decreased the pain threshold of non-inflamed hindpaws (300 nmol). (2) (±)-SKF38393 hydrochloride ((±)-1-phenyl-2,3,4,5-tetrahydro-(1 H)-3-benzazepine-7,8-diol hydrochloride), a dopamine D 1 receptor agonist, had no effect on either hindpaw, even at a higher dose (300 nmol); R(+)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrochloride ( R(+)-SCH23390 hydrochloride), a dopamine D 1 receptor antagonist, induced anti-hyperalgesia in the inflamed hindpaws (300 nmol). The present results suggest that the dopaminergic system in the spinal cord is involved in the central modulation of inflammatory hyperalgesia, and that the different effects are probably induced by different receptors.

Effects of dopaminergic agents on carrageenan hyperalgesia in rats

The present study explored the role of central dopaminergic transmission in a model of carrageenan-induced inflammatory pain by examining the effects of selective agonists and antagonists of dopamine receptors. The results were as follow: (1) LY171555 ( trans-(−)-4a R-4,4a,5,6,7,8,8a,9-Octahydro-5-propyl-1 H-pyrazolo[3,4-g]quinoline hydrochloride), dopamine D 2 receptor agonist, produced anti-hyperalgesia or hypoalgesia in the inflamed hindpaws and non-inflamed hindpaws, respectively; spiperone hydrochloride (8-[4-(4-Fluorophenyl)-4-oxobutyl]-1-phenyl-1,3,8-triazaspiro[4,5]decan-4-one hydrochloride), dopamine D 2 receptor antagonist, decreased the pain threshold of the non-inflamed hindpaws. (2) (±)-SKF38393 hydrochloride ((±)-1-Phenyl-2,3,4,5-tetrahydro-(1 H)-3-benzazepine-7,8-diol hydrochloride), dopamine D 1 receptor agonist, produced anti-hyperalgesia or hypoalgesia when administered in a high dose (600 nmol), and decreased the pain threshold of non-inflamed hindpaws when administered in a low dose (150 nmol); R(+)-SCH23390 hydrochloride ( R(+)-7-Chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrochloride), dopamine D 1 receptor antagonist, induced anti-hyperalgesia or hypoalgesia, respectively. The present study suggests that the dopaminergic system is involved in the central modulation of inflammatory hyperalgesia, and that the different effects are probably induced by the different receptors.

Motor effects of (−)-OSU6162 in primates with unilateral 6-hydroxydopamine lesions

The effects of the novel compound, (−)-OSU6162 (( S)-(−)-3-methylsulfonylphenyl-1-propylpiperidine), on rotational behavior induced by dopamine receptor agonists was investigated in common marmosets ( Callithrix jacchus) with unilateral 6-hydroxydopamine lesions. (−)-OSU6162 per se displayed no effect on the animals' behavior. On the other hand, pretreatment with (−)-OSU6162 attenuated rotational behavior induced by apomorphine (apomorphini hydrochloridum), l-DOPA (3,4-dihydroxyphenylalanine), and the dopamine D2 receptor agonist, quinpirole ( trans-(−)-4 aR-4,4 a,5,6,7,8,8 a,9-octahydro-5-propyl-1 H-pyrazolol[3,4- g]quinoline hydrochloride), without inducing motor impairment such as akinesia or dystonia. In addition, treatment with (−)-OSU6162 for 5 consecutive days almost completely abolished the rotational behavior provoked by apomorphine and produced a transient subsensitization of such apomorphine-induced effects after it was discontinued. Moreover, pretreatment with (−)-OSU6162 in two monkeys augmented the rotational behavior elicited by the dopamine D1 receptor agonists, SKF-81297 ( R(+)-6-chloro-7,8,dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide) and A-77636 ((−)-(1 R,3 S)-3-adamantyl-1-(aminomethyl)-3,4-dihydro-5,6-dihydroxy-1 H-2-benzopyran hydrochloride). The findings indicate that (−)-OSU6162 can exert indirect state-dependent effects that differentially affect dopamine D1 and dopamine D2 receptor agonist-induced behavior.

Dopaminergic modulation of rat pup ultrasonic vocalizations

The dopamine D 1 receptor agonist, R(+)-6-chloro-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide (SKF 81297), the dopamine D 2/D 3 receptor agonist, trans-(−)-4 aR-4,4 a,5,6,7,8,8 a,9-octahydro-5-propyl-1 H-pyrazolo[3,4- g]quinoline hydrochloride (quinpirole), and the dopamine D 3 receptor agonist, (±)-7-hydroxy-dipropylaminotetralin hydrobromide (7-OH-DPAT) all reduced the frequency of isolation-induced infant rat ultrasonic vocalizations and lowered body temperature when compared to saline-injected controls. Ultrasonic vocalization rate was not affected by either the dopamine D 1 receptor antagonist, R(+)-2,3,4,5-tetrahydro-8-iodo-3-methyl-5-phenyl-1 H-3-benzazepin-7-ol hydrochloride (SCH 23390) or the dopamine D 2/D 3 receptor antagonist, S(−)-raclopride- l-tartrate (raclopride) when given alone, nor did these antagonists block the ultrasonic vocalization reductions caused by the dopamine D 1 receptor agonist or the dopamine D 2/D 3 receptor agonist. The dopamine D 2/D 3 receptor antagonist but not the dopamine D 1 receptor antagonist blocked the dopamine D 3 receptor agonist's ultrasonic vocalization reduction. SKF 81297 reduced general activity while quinpirole and 7-OH-DPAT increased activity. Raclopride reversed quinpirole's reduction in body temperature, as well as 7-OH-DPAT's effects on body temperature, ultrasonic vocalizations, and activity. These results indicate that dopamine D 1, D 2/D 3, and D 3 receptor agonists all reduce ultrasonic vocalizations by as yet undetermined mechanisms.

BU-224 produces spinal antinociception as an agonist at imidazoline I 2 receptors

In this electrophysiological study, the effect of BU-224 [2-(4,5-dihydroimidazol-2yl)-quinoline hydrochloride)], a novel high affinity imidazoline I 2 receptor ligand, was tested on the responses of nociceptive neurones in the spinal dorsal horn. When applied spinally, akin to an intrathecal application (i.t.), BU-224 (5-250 μg) reduced the nociceptive responses of dorsal horn neurones, producing a dose-dependent inhibition of C-fibre evoked responses, postdischarge and wind-up of the cells. A complete block of the antinociceptive effects was produced when idazoxan (100 μg), with both α 2-adrenoceptor and imidazoline I 2 receptor antagonist actions, was administered i.t. 10 min prior to the maximal dose of BU-224 tested. The nonselective α 2-adrenoceptor antagonist, yohimbine (150 μg) only partially attenuated the inhibitory effects of BU-224 when administered i.t. 10 min prior. The highly selective α 2-adrenoceptor antagonist, atipamezole (100 μg) produced no greater reversal than yohimbine under the same conditions. Although BU-224 has been reported to possess high affinity for imidazoline I 2 receptors, a minor action at spinal α 2-adrenoceptor receptors cannot be discounted. These results demonstrate that BU-224 is an agonist and that imidazoline I 2 receptors, present in the dorsal horn, might play a role in spinal nociception, although further studies are needed to fully elucidate their functional roles.

Threshold of dopamine content and D1 receptor stimulation necessary for the expression of rotational behavior induced by D2 receptor stimulation under normo and supersensitive conditions.

We measured the minimum amount of endogenous dopamine (EDA), necessary for the expression of rotational behavior induced by D2 receptor stimulation in striatal or medial forebrain bundle (MFB) lesioned rats. We correlated these results with the minimum dose of D1 receptor agonists needed to substitute EDA in its permissive role for D2 motor effects to take place. Rats with unilateral quinolinic acid (QA) striatal or 6-hydroxydopamine (6-OHDA) MFB lesions were given increasing doses of the tyrosine hydroxylase inhibitor alpha-methyl-para-tyrosine (AMPT) in combination with a fixed dose of the D2 receptor agonist quinpirole (trans-(-)-4aR-4,4a,5,6,7,8,8a,9-Octahydro-5-propyl-1H-pyrazolo(3, 4-g) quinoline hydrochloride) and tested for rotational behavior. The animals were later sacrificed and striata removed; EDA was measured by high performance liquid chromatography (HPLC). Rotational responses were abolished by increasing doses of AMPT inducing a stepwise depletion of EDA. EDA content and rotational behavior to D2 stimulation showed a high degree of correlation. There was an abrupt reduction in rotational behavior at dopamine levels of 50-60% of controls in both animal models. In addition, striatal or MFB lesioned rats which were maximally depleted of dopamine by AMPT pretreatment received a fixed dose of quinpirole and then challenged with increasing doses of a D1 receptor agonist SKF 38393 ((+/-)-1-Phenyl-2,3,4,5-tetrahydro-(1H)-3-benzazepine-7,8-diol hydrochloride). Rotational behavior was restored by SKF 38393 in both animal models in a dose-dependent fashion. Our results confirm the need for simultaneous D1/D2 stimulation in the generation of rotational behavior in both animal models. Moreover, they demonstrate the existence of a threshold level of D1 stimulation necessary to exert its permissive role on D2 mediated responses.

Role of lipoxygenase metabolites in platelet-activating factor- and antigen-induced bronchial hyperresponsiveness and eosinophil infiltration

The effect of a novel leukotriene B4 receptor antagonist N-[5-[[8-(1-hydroxy-2-phenyl)ethyl]dibenzofuran-2-yl]-5-hydroxypentanoyl] pyrrolidine (PF 10042) has been evaluated in comparison with 2-[3-(1-hydroxyhexyl)phenoxymethyl]quinoline hydrochloride (PF 5901), a specific inhibitor of the 5-lipoxygenase pathway of arachidonic acid metabolism, against platelet activating factor (PAF) and allergen induced bronchial hyperresponsiveness and pulmonary eosinophil infiltration in the guinea pig. PF 10042 significantly displaced radiolabelled [3H]leukotriene B4 from binding sites on human neutrophils with an EC50 of 3 μM. PF 10042 (100 mg/kg, i.p.) significantly inhibited PAF and allergen induced bronchial hyperresponsiveness without reducing the concomitant eosinophil infiltration, whereas PF 5901 (100 mg/kg, p.o.) significantly inhibited both PAF and allergen induced bronchial hyperresponsiveness and eosinophil infiltration. We suggest from these results that PAF and allergen induced bronchial hyperresponsiveness may be secondary to the release of leukotriene B4, but this lipoxygenase metabolite does not contribute significantly to the observed eosinophil infiltration.

Role of lipoxygenase metabolites in platelet-activating factor- and antigen-induced bronchial hyperresponsiveness and eosinophil infiltration

The effect of a novel leukotriene B 4 receptor antagonist N-[5-[[8-(1-hydroxy-2-phenyl)ethyl]dibenzofuran-2-yl]-5-hydroxypentanoyl] pyrrolidine (PF 10042) has been evaluated in comparison with 2-[3-(1-hydroxyhexyl)phenoxymethyl]quinoline hydrochloride (PF 5901), a specific inhibitor of the 5-lipoxygenase pathway of arachidonic acid metabolism, against platelet activating factor (PAF) and allergen induced bronchial hyperresponsiveness and pulmonary eosinophil infiltration in the guinea pig. PF 10042 significantly displaced radiolabelled [ 3H]leukotriene B 4 from binding sites on human neutrophils with an EC50 of 3 μM. PF 10042 (100 mg/kg, i.p.) significantly inhibited PAF and allergen induced bronchial hyperresponsiveness without reducing the concomitant eosinophil infiltration, whereas PF 5901 (100 mg/kg, p.o.) significantly inhibited both PAF and allergen induced bronchial hyperresponsiveness and eosinophil infiltration. We suggest from these results that PAF and allergen induced bronchial hyperresponsiveness may be secondary to the release of leukotriene B 4, but this lipoxygenase metabolite does not contribute significantly to the observed eosinophil infiltration.

Effect of a 5‐lipoxygenase inhibitor and leukotriene antagonist (PF 5901) on antigen‐induced airway responses in neonatally immunized rabbits

1. The effect of a single intratracheal dose (10 mg) of PF 5901 (2-[3(1-hydroxyhexyl) phenoxymethyl] quinoline hydrochloride, a specific inhibitor of the 5-lipoxygenase pathway of arachidonic acid metabolism and a leukotriene D4 antagonist) on airway changes induced in response to Alternaria tenuis aerosol challenge was assessed in adult rabbits neonatally immunized. Leukotriene generation was determined in vivo by measuring leukotriene B4 (LTB4) levels in bronchoalveolar lavage (BAL) fluid and ex vivo by measuring calcium ionophore-stimulated production of LTB4 in whole blood. 2. While PF 5901 (10 mg) had no significant effect on the acute bronchoconstriction induced by antigen, this dose was sufficient to inhibit significantly the increase in airway responsiveness to inhaled histamine 24 h following antigen challenge (P < 0.05). 3. Total leucocyte infiltration into the airways induced by antigen, as assessed by bronchoalveolar lavage, was significantly inhibited by pretreatment with PF 5901 (10 mg). However, the pulmonary infiltration of neutrophils and eosinophils induced by antigen was unaltered by prior treatment with PF 5901 (10 mg). 4. PF 5901 (10 mg) had no effect on ex vivo LTB4 synthesis in whole blood. However, the antigen-induced increase in LTB4 levels in BAL 24 h following challenge was significantly inhibited (P < 0.05). 5. We suggest from the results of the present study that the antigen-induced airway hyperresponsiveness to inhaled histamine in immunized rabbits is mediated, at least in part, by products of the 5-lipoxygenase metabolic pathway, and is not dependent on the extent of eosinophil or neutrophil influx into the airway lumen.

Dopaminergic modulation of pilocarpine-induced motor seizures in the rat: The role of hippocampal D 2 receptors

This study examined the role of hippocampal dopamine D 2 receptors in the genesis of limbic seizures induced by muscarinic agonists in the rat. Pilocarpine, 600 mg/kg, elicited rapid and usually fatal convulsions. These were not affected by focal injections of saline (1 μl) into both hippocampi. Pretreatment of the dorsal, but not the lateral hippocampus, with the D 2 agonist trans-(+)-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-2H-pyrazolo-(3,4-g)quinoline hydrochloride (LY 171555, 2 μg per side), did not alter the frequency of pilocarpine-induced convulsions, but significantly delayed their appearance and reduced their intensity. LY 171555 similarly increased the latency of seizures induced by focal hippocampal injection of carbachol (100 μg), without changing the frequency or the severity. The selective D 2 antagonist raclopride, injected dorsally into both hippocampi dose-dependently facilitated motor seizures evoked by pilocarpine (100 mg/kg), the cholinomimetic at this dose being ineffective as a convulsant in saline-treated animals. Intrahippocampal administration of the D 1 agonist 2,3,4,5-tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine hydrochloride (SKF 38393, 2 μg per side) did not facilitate pilocarpine seizures and did not potentiate the proconvulsant action of raclopride. These data demonstrate that activation of the dopaminergic system, via D 2 receptors in the dorsal hippocampus, is capable of protecting the animal against limbic motor seizures arising from excessive muscarinic stimulation of the hippocampus. Since the blockade of D 2 receptors in the hippocampus markedly lowered the seizure threshold to pilocarpine, this would suggest that the dopaminergic input to the hippocampus is normally tonically active and functions physiologically to prevent epileptogenesis.

Stereoselective synthesis and optical resolution of chiral calix[4]arenes with mixed ligating functionalities

Exhaustive alkylation of syn-proximal bis[(2-pyridylmethyl)oxy]calix[4]arene 1 with t-butyl bromoacetate or 2-(chloromethyl)quinoline hydrochloride in the presence of Cs 2CO 3 affords selectively a new type of inherently chiral calix[4]arenes 2a,b in the partial cone conformation. (±) 2b has been resolved into its optical antipodes by an HPLC method.

Anticonvulsant effect of striatal dopamine D 2 receptor stimulation: Dependence on cortical circuits?

In the pilocarpine model of epilepsy, dopamine can either inhibit (via D 2 receptors) or facilitate (via D 1 receptors) the spread of limbic motor seizures. The anticonvulsant action of D 2 receptor activation has been localized to the anterior striatum, but disappears if excessive damage is caused to the overlying cerebral cortex. This study examines the possiblity that the corticostriatal projection is involved in the anticonvulsant response to striatal D 2 receptor stimulation, by comparing the seizure-protecting efficacy of intrastriatal trans-( + )-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-2H-pyrazolo-(3,4-g)quinoline hydrochloride (LY 171555) in control rats, and in rats bearing discrete bilateral kainic acid lesions of the cerebral cortex. The results show that neurotoxin injection induces a punctate lesion of the primary motor area of the cortex in each hemisphere, with no injury to the underlying caudate-putamen, or to more distant structures such as the hippocampus. The lesion, however, was sufficient to abolish the protective effect of intrastriatal LY 171555 against pilocarpine challenge. To explain these findings, an interplay between nigrostriatal dopaminergic and corticostriatal glutamatergic neurons is proposed, in which the anticonvulsant tendency of the excitatory amino acid is accentuated by dopamine, probably by acting on D 2 receptors which facilitate the release of glutamate from axon terminals.

NIK-247 Blocks Voltage-Dependent Ionic Currents in Crayfish Axon.

NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-1H-cyclopenta[b]-quinoline hydrochloride hydrate), an acetylcholinesterase inhibitor, is structurally related to 4-aminopyridine (AP). Its effects on ionic currents were examined in the artificial node of the crayfish axon under voltage-clamp. When applied externally, NIK-247 reversibly suppressed both inward and outward currents. Effects on K currents were further studied in the presence of tetrodotoxin. NIK-247 suppressed the K current dose-dependently, but with an IC50 at of 10(-3) M. THA (9-amino-1,2,3,4-tetra-hydroacridine hydrochloride hydrate), a related inhibitor, similarly suppressed the K current with an IC50 of 5 x 10(-4) M, in comparison with 3-AP and 4-AP which had IC50's of 3 x 10(-5) M and at 10(-5) M, respectively. Furthermore, NIK-247 (and THA) suppressed the K current uniformly for the whole time course, whereas AP the AP's suppressed mainly the fast activating and inactivating K current with a voltage- and frequency-dependent recovery. Therefore, NIK-247 and THA seem to be neither potent nor very specific as ionic channel blockers. With respect to the K current, however, they clearly differ from the AP's in their mode of suppression.

NIK-247 Blocks Voltage-Dependent Ionic Currents in Crayfish Axon

NIK-247 (9-amino-2,3,5,6,7,8-hexahydro-lH-cyclopenta[b]-quinoline hydrochloride hydrate), an acetylcholinesterase inhibitor, is structurally related to 4-aminopyridine (AP). Its effects on ionic currents were examined in the artificial node of the crayfish axon under voltage-clamp. When applied externally, NIK-247 reversibly suppressed both inward and outward currents. Effects on K currents were further studied in the presence of tetrodotoxin. NIK-247 suppressed the K current dose-dependently, but with an IC50 at of 10-3 M. THA (9-amino-1,2,3,4-tetra-hydroacridine hydrochloride hydrate), a related inhibitor, similarly suppressed the K current with an IC50 of 5 × 10-4 M, in comparison with 3-AP and 4-AP which had IC50’s of 3 × 10-5 M and at 10-5 M, respectively. Furthermore, NIK-247 (and THA) suppressed the K current uniformly for the whole time course, whereas AP the AP’s suppressed mainly the fast activating and inactivating K current with a voltage- and frequency-dependent recovery. Therefore, NIK-247 and THA seem to be neither potent nor very specific as ionic channel blockers. With respect to the K current, however, they clearly differ from the AP’s in their mode of suppression.

Radiation induced grafting of methacrylic acid onto silk for the immobilization of antimicrobial drug for sustained delivery

AbstractMedical grade black braided silk suture and pure mulberry silk twisted yarn were grafted with methacrylic acid (MAA) using 60Co gamma radiation. The effect of various synthesis conditions on the grafting was studied. The addition of methanol in water has a marked effect on the degree of grafting, maximum yield of grafting was obtained in an equivolume mixture of water‐methanol. The percent grafting increased with the increase in the monomer concentration and in total radiation. For a constant total dose, grafting was found to be higher at lower dose rates. The order of the dependence of the rate of grafting on the dose rate was found to be 0.53 and 0.56 for medical grade black braided silk suture samples and mulberry silk twisted yarn samples respectively. The immobilization of an antimicrobial drug, 8‐hydroxy quinoline (8‐HQ) hydrochloride on the grafted pure silk for sustained delivery, its release in vitro and its antimicrobial activity were also studied. The percentage of 8‐HQ immobilized onto various grafted silk samples increased with the increase in the degree of grafting. The release of the drug in distilled water was sustained for 32 days. 8‐HQ was found to be active against both gram‐positive and Gram‐negative bacteria.

Structural and Magnetic Investigation of BIS (Quinolinium) BIS (Maleonitrile Dithiolato) Cuprate (II) - (Quin)2Cu(mnt)2

Abstract The title compound (Quin)2Cu(mnt)2 was synthesized by metathesis of the sodium salt of Cu(mnt)2 2- with quinoline hydrochloride, and its structural and magnetic properties were examined. The X-ray crystal structure reveals the segregated stacking of the Cu(mnt)2 2- anions and the quinolinium cations and indicates anisotropic properties. The magnetic susceptibility studies show that the exchange interaction is very weak as the Curie-Weiss fit holds down to 2.5K. The dynamics of the exchange interaction as probed by EPR linewidth analysis yield detailed information about the strengths of the various magnetic interactions.

Condensation of 2-amino-3, 4, 5, 6-tetrahydroimidazo[4,5,1-ij]quinolinium and 2-amino-2-pyrrolinium salts with ?- dike tones

The corresponding 12,l,2,3-tetrahydropyrimido[2′,1′∶2,3]imidazo[4,5,1-ij]quinolinium and 7,8-dihydro-6H-pyrrolo[1,2-a]pyrimidinium salts were obtained by the condensation of 2-amino-3,4,5,6-tetrahydroimidazo[4,5,1-ij]quinoline hydrochloride and 2-amino-2-pyrroline hydrochloride with β-diketones. The structures of the products of condensation with unsymmetrical diketones were determined from their PMR spectra.

Studies on the synthesis of aminoquinoline derivatives. VII. Synthesis of imidazo(1,2-alpha)quinoline derivatives

Nucleophilic reaction of the methyl derivatives of 2-chloroquinoline with aminoethanol, ε-aminocaproic acid, and its ester was examined. ε-Aminocaproic ester was extremely difficult to react, aminoethanol reacted with better yield than 3-aminopropanol, and reaction with ε-aminocaproic acid failed to give any reaction product. The hydroxyl group in ω-position of 2-(2-hydroxyethylamino) quinoline, obtained by reaction with aminoethanol, was chlorinated to obtain the methyl derivative of 2-(2-chloroethylamino)-quinoline hydrochloride. Neutralization of this hydrochloride by addition of saturated sodium hydrogencarbonate solution to pH 7.0-7.1 afforded some crystals which were found to be not the liberated base but 2, 3-dihydro-1H-imidazo [1, 2-α] quinolinium chloride, produced by the new formation of a five-membered ring between the chlorinated carbon atom and the non-conjugated electron pairs in the sp orbital of the ring nitrogen during neutralization. This quaternary salt was heated with 10% sodium hydroxide solution and a pseudo base possessing a hydroxyl in 3a-position was obtained.

Cholestanol esters of amino acids.

Abstract The cholestanol (5α-cholestan-3β-ol) esters of amino acids were synthesized with an interest for their possible biochemical activities. The cholestanol esters of glycine, l-alanine, β-alanine, l-leucine and l-aspartic acid were synthesized by a direct fusion of the two components under the passing of hydrogen chloride through the reactants. That of glutamic acid was prepared by using quinoline hydrochloride as a solvent. From the condensation product of aspartic acid and cholestanol, mono- and di-ester were isolated. The monocholestanol ester of aspartic acid was also synthesized by the Gabriel process.

The interaction between quinoline hydrochloride and sodium docosyl sulphate at the air-water interface at 25°C

The interaction between quinoline hydrochloride and sodium docosyl sulphate at the air-water interface at 25°C