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PubMed1976

The metabolism of (1-14C) stearic acid in rat testicular tissue.

(1) The metabolism of stearic acid was studied in vivo following intratesticular injection of [1-14C] stearate. Soon after injection 14C activity was found mainly in the free fatty acid pool. This was followed at later time periods by transfer of label primarily to the phosphatide pool. During each time period significant amounts of label were recovered at 14CO2. (2) Analysis of 14C-labeled fatty acids from the injected testes demonstrated an initial rapid rate of oxidation and desaturation of [1-14C] stearate followed by a slower steady state rate. It was concluded that the initial rate was due to the rapid turnover of the highly labeled free fatty acid pool followed by a much slower rate as [14C] stearate was esterified to the more metabolically stable phospholipids. Elongation of the labeled stearic or its desaturated derivative was not observed. (3) The rate of desaturation in vitro of stearic acid was measured in microsomal preparations from rat testes and found to be 12.0 +/- 0.5 pmol/min/mg compared to the estimated in vivo value of 22 pmol/min/mg and the value of 390 pmol/min/mg for hepatic microsomal desaturase.

Animals↗
PubMed1981

The suitability of different acyl acceptors as substrates for the acyl-Coa : 2-acyl-sn-glycero-3-phosphorylcholine acyltransferase in rat liver microsomes.

The fatty acid selectivity of the acyl-CoA : 2-acyl-sn-glycero-3-phosphorylcholine acyltransferase towards different acyl acceptors was studied in rat liver microsomes. The individual molecular species of 2-acylglycerylphosphorylcholine tested as enzyme substrates contained either palmitate, stearate, oleate, linoleate, linolenate or arachidonate with an equimolar mixture of [14C]palmitoyl-CoA plus [3H]stearoyl-CoA serving as the acyl donor. At 2-acyl-sn-glycero-3-phosphorylcholine concentrations of 16 or 64 microM, the various acyl acceptors gave generally similar reactivities, although reaction velocities with the linoleoyl, linolenoyl or arachidonoyl species were moderately greater than those with 2-stearoyl-sn-glycero-3-phosphorylcholine. Regardless of the acyl acceptor tested, little preference towards either palmitoyl-CoA or stearoyl-CoA was indicated at 64 microM 2-acyl-sn-glycero-3-phosphorylcholine whereas a distinct preference for stearate over palmitate (by 1.9--2.6-fold) was exhibited when a lower concentration (16 microM) of the acceptor was employed. The results support the potential importance of the acyl-CoA : 2-acyl-sn-glycero-3-phosphorylcholine acyltransferase for the synthesis of 1-stearoyl 2-unsaturated species of phosphatidylcholine. However, it cannot independently account for the varying palmitate : stearate ratios in the 1-position of this phospholipid when different unsaturated fatty acids reside in the 2-position.

Acyl Coenzyme A↗
PubMed1984

Regulation of intracellular arachidonate in normal and stressed endothelial cells.

The uptake of arachidonate and stearate from serum-free media by endothelial cells was investigated over a 48 h period. Arachidonate was rapidly incorporated into both the phospholipids and triacylglycerols. Triacylglycerol incorporation reached a maximum at 2 h and then rapidly declined with a concomitant increase in phospholipid incorporation. High initial arachidonate incorporation into phosphatidylcholine was followed by a partial transfer of that arachidonate to phosphatidylethanolamine. In contrast, stearate was slowly incorporated into all of the phospholipids and was not incorporated into the triacylglycerols. Cells stimulated with A23187 for 24 h cleaved stearate from all the phospholipids equally, whereas more arachidonate was cleaved from phosphatidylethanolamine than from the other phospholipids. Released arachidonate was both metabolized and reacylated into the triacylglycerols. Our results suggest that triacylglycerols serve as a modulator of intracellular arachidonate concentrations in endothelial cells.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Evidence that remodeling of the fatty acids of phosphatidylcholine is regulated in isolated rat hepatocytes and involves both the sn-1 and sn-2 positions.

The remodeling of the fatty acyl moieties of phosphatidylcholine (PC) has been studied in choline-deficient and choline-supplemented hepatocytes prepared from a choline-deficient rat. Choline-deficient hepatocytes were prelabeled with [Me-3H]choline for 30 min and subsequently incubated for up to 12 h in the presence or absence of choline. Analysis of the molecular species of PC from choline-deficient cells showed that, at the end of the pulse, approx. 75% of the label was incorporated into palmitate-containing species and only approx. 16% of the labeled species contained stearate. During the chase period there was a redistribution of label and after 12 h approx. 56% of the total radioactivity was associated with palmitate containing species and 37% was recovered in stearate-containing species. A similar distribution of radioactivity was observed in choline-supplemented cells. Measurement of the specific radioactivity of the major molecular species of PC was consistent with a precursor-product relationship between palmitate-containing species and stearate-containing species with arachidonate or linoleate on the sn-2 position. A model is presented which takes into account remodeling of both the sn-1 and sn-2 positions of PC.

Animals↗
PubMed1976

Identification of isomeric doxyl stearic acids by gas-liquid chromatography and mass spectrometry.

Direct probe and GC/MS spectra were determined for the isomeric 4- to 16-doxyl stearic acids and their methyl and silyl esters in pure form and in mixture with natural fatty acids and their esters. The base peak for all free and esterified doxyl stearic acids was at m/e 281. The methyl esters of all isomers gave nearly identical fragments in the high mass regions having M+ at m/e 398 with intensities of 2-3%. The isomers were identified on the basis of the fragments retaining the doxyl group, which had positive charge and were different for each compound. It was shown that the fragment m/e 281 may be used to identify and quantitate the stearate derivatives in presence of natural fatty acids. The silyl esters of the doxyl stearates gave complex mass spectra. The isomeric doxyl stearates were resolved by GLC on 3 ft. glass columns containing 1% SE-30 packing as methyl esters.

Electron Spin Resonance Spectroscopy↗
PubMed1995

Loratadine administered concomitantly with erythromycin: pharmacokinetic and electrocardiographic evaluations.

OBJECTIVE: To evaluate the effects of coadministration of loratadine and erythromycin on the pharmacokinetics and electrocardiographic repolarization (QTc) pharmacodynamics of loratadine and its metabolite descarboethoxyloratadine in healthy volunteers. METHODS: Twenty-four healthy volunteers were studied in a prospective, double-blind crossover design while confined in a Clinical Research Center. The primary pharmacodynamic end point of the study was the difference between baseline and day 10 mean QTc intervals obtained from surface electrocardiograms. Plasma concentrations of loratadine, descarboethoxyloratadine, and erythromycin were measured on treatment day 10 for pharmacokinetic analysis. Subjects received in random sequence the following three treatments for 10 consecutive days during three separate study periods: 10 mg loratadine every morning plus 500 mg erythromycin stearate every 8 hours, or 10 mg loratadine every morning plus placebo every 8 hours, or placebo every morning plus 500 mg erythromycin stearate. RESULTS: Concomitant administration of loratadine and erythromycin was associated with increased plasma concentrations of loratadine (40% increase in area under the plasma concentration-time curve [AUC]) and descarboethoxyloratadine (46% increase in AUC) compared with loratadine alone. Analysis of variance showed no difference between the treatment groups in effect on QTc intervals compared with baseline, and no significant change from baseline was observed. No clinically relevant changes in the safety profile of loratadine were observed, and there were no reports of sedation nor syncope. CONCLUSION: Although concomitant administration of loratadine and erythromycin was associated with increased plasma concentrations of loratadine and descarboethoxyloratadine, no clinically relevant changes in the safety profile of loratadine were observed. In this study, 10 mg loratadine administered orally for 10 consecutive days was well tolerated when coadministered with therapeutic doses of erythromycin stearate.

Adult↗
PubMed1996

Release of CuPTSM from human serum albumin after addition of fatty acids.

Copper-62 labeled pyruvaldehyde bis (N4-methyl-thiosemicarbazonato) copper(II), CuPTSM, has been used to probe tissue perfusion by means of positron emission tomography. Despite promising results from animals, problems have been encountered in the use of 62CuPTSM to quantitate regional myocardial blood flow in humans. Ultrafiltration and plasma/erythrocyte partitioning studies with radiotracer have previously shown that CuPTSM is bound much more strongly by human serum albumin (HSA) than by dog serum albumin (DSA), limiting its ability to freely diffuse from blood into tissue. In this study, it is confirmed by electron spin resonance (ESR) that CuPTSM strongly binds to HSA with an apparent gparallel value of 2.12 and an apparent Aparallel value of 186 G. It is also shown that both spin-labeled stearic acid (5-SASL) and nonspin-labeled stearate inhibit CuPTSM binding to HSA. CuPTSM is completely released from HSA when the ratio of 5-SASL to HSA is 5:1. When pure sodium stearate is used, the binding of CuPTSM significantly decreased, about 73% of CuPTSM is released with a ratio of 4:1 stearate to HSA. These results highlight a means of liberating CuPTSM from HSA.

Electron Spin Resonance Spectroscopy↗
PubMed1985

The importance of the stearoyl-CoA desaturase system in octadecenoate metabolism in the Morris hepatoma 7288C.

The sources of octadecenoic acid (18:1) and the importance of the stearoyl-CoA desaturase system in maintaining elevated levels of this fatty acid in the Morris hepatoma 7288C have been investigated. Sterculic acid, an inhibitor of the stearoyl-CoA desaturase system, when added to the culture medium, inhibited the production of monoenoic fatty acids through de novo synthesis by 90% while the production of saturated fatty acids and cholesterol was unaffected. Sterculic acid also inhibited 18:1 formation through desaturation of exogenous stearate (18:0) by 80%. These results indicate that the stearoyl-CoA desaturase system is responsible for most, if not all, of the 18:1 produced within these cells and that an alternate, sterculic acid-insensitive, pathway for 18:1 biosynthesis is not functioning in this cell line. Measurements of fatty acid synthesis, using 3H2O, show that de novo synthesis accounts for approx. 30% of the cellular 16:1 and 18:1 mass, while contributing 63% and 95% of the stearate and palmitate mass, respectively. Cells grown in the presence of sterculic acid displayed a 50% decrease in 18:1 levels while levels of both palmitate and stearate increased. These effects were maximal at 20-30 microM sterculate. Polyunsaturate levels were unaffected. The 50% decrease in 18:1 levels in treated cells could be completely accounted for by the inhibition of de novo 18:1 biosynthesis and the inhibition of exogenous 18:0 desaturation. This enzyme system, although low in activity when measured in this tissue, is responsible for a major portion of the 18:1 observed in these cells.

Animals↗
PubMed1980

Incorporation of saturated and cis- and trans-unsaturated long chain fatty acids in rat myocytes and increased susceptibility to arrhythmias.

Neonatal rat heart myocytes cultured for 3 days in fatty acid-enriched (5 X 10(5) M stearate, oleate, elaidate, linoleate, linoelaidate or arachidonate at a 3 : 1, fatty acid (FA/albumin ratio) were analyzed by high-pressure liquid chromatography (HPLC) for the FA content of their neutral lipid, glyco-cardiolipid and phospholipid fractions and were tested for their susceptibility to arrhythmias produced by hypoxic/normoxic medium changes. Increases in the relative amount of FA in the above lipid fractions were generally in the order: elaidate = linoelaidate greater than linoleate = arachidonate greater than stearate = oleate. Cell morphology was unaffected by such treatment, but the cultures were more susceptible to induced arrhythmias. Cultures enriched with trans-FA, elaidate or linoelaidate, became markedly arrhythmic; arrhythmias in stearate-enriched cultures were of short duration; whereas the other FA produced intermediate increases. Susceptibility to arrhythmias could not be correlated with polyunsaturated fatty acid (PUFA/saturated fatty acid (SATFA) ratios of FA in the phospholipid fraction.

Animals↗
PubMed1990

ESR studies of stearic acid binding to bovine serum albumin.

The ESR spectra of a series of chain-labelled doxyl stearic acids (5-, 7-, 12- and 16-DSA) and doxyl methyl stearates (5-, 7-, 12- and 16-DMS) bound to the high-affinity binding sites of bovine serum albumin (BSA) have been analyzed using nonlinear least-squares fitting of slow-motional ESR stimulation. The motional analysis reveals that the rotational diffusion of these stearates around the axis perpendicular to the long hydrocarbon chain is greatly hindered, suggesting that they are held tightly in a channel of the protein. Comparison of the isotropic hyperfine splitting, A0, among each series shows that 5- and 16-DSA and 16-DMS have larger A0 values than the other spin labels. In addition, labels at the 16-C position of both DSA and DMS exhibit significantly increased motion relative to the other positions. These observations suggest that the channel starts at 5-C of the chain and ends somewhere between 13-C and 15-C, leading to an estimate of 11 +/- 1 A for the length of the channel. The methyl stearate labels exhibit significantly faster rotation around the chain axis than the analogous stearic acid labels, suggesting a double hydrogen-bonding mechanism for fatty acid binding to BSA. The ability of the acid to form two hydrogen bonds apparently fixes it more rigidly in the protein, preventing rotation about either single hydrogen bond. A double-hydrogen bonding mechanism is most consistent with the formation of a salt bridge between the negatively charged carboxylate of the acid and either a positively charged guanidino group of arginine, or the positively charged omega-amino groups of two lysine residues. An ESR study of the pH dependence of DSA binding indicates that salt bridge formation with lysine is responsible for at least some of the long chain fatty acid binding sites of BSA.

Amino Acid Sequence↗
PubMed1992

Sex and dietary fat modulate hepatic prostaglandin F2 alpha in F344/N rats.

The study was designed to determine whether sex and fat calories altered hepatic prostaglandin (PG) F2 alpha status; a factor which may reflect susceptibility to cancer development. For 4 weeks, groups of 8 male and 8 female F344/N rats were fed diets with 9% of energy (en%) from linoleate and 15.5, 20, 30 or 40 en% fat. Females had greater hepatic stearate, arachidonate and PGF2 alpha whereas males had greater hepatic myristate, palmitate and oleate. Females also had greater plasma stearate levels. Greater hepatic arachidonate may have stimulated PG production in females. Hepatic oleate increased and hepatic palmitate decreased with increasing en% fat (p < 0.05). Hepatic stearate was greater and hepatic linoleate less when 40 en% fat was fed compared with other levels of dietary fat (p < 0.05). Plasma oleate was greater at 30 or 40 en% fat than at lower levels of fat, whereas plasma linoleate was less at 40 en% than at 15.5% en% fat. The ability of a 30 en% fat diet, containing equal proportions of linoleate and oleate, to suppress hepatic PG production may be related to the effects of dietary fat content and composition on plasma fatty acid profiles. Because suppressed PG production has been linked with suppression of cancer development, dietary recommendations to consume 30 en% fat with a P:M ratio of 1:1 may be cancer-protective.

Animals↗
PubMed2004

Separation of geometric isomers of native lutein diesters in marigold (Tagetes erecta L.) by high-performance liquid chromatography-mass spectrometry.

Lutein is found in many foods; the richest and purest plant source is marigold flower (Tagetes erecta L.). In this plant, lutein is in the form of saturated fatty acid diesters. By using a binary mobile phase consisting of ethyl acetate and acetonitrile-methanol (9:1), improved separation was achieved on a C18-bonded phase. The unique absorption of lutein cis isomers at 330nm was used in combination with MS to identify the novel cis-lutein isomeric dimyristate, myristate-palmitate, dipalmitate, and palmitate-stearate diesters, as well as the rare combinations of both trans- and cis-lutein laurate-palmitate and trans- and cis-lutein myristate-stearate. The presence of the all-trans-lutein laurate-myristate, dimyristate, myristate-palmitate, palmitate-stearate, and distearate diesters, reported by others, was also confirmed.

Chromatography, High Pressure Liquid↗
PubMed2004

Particle interaction of lubricated or unlubricated binary mixtures according to their particle size and densification mechanism.

The aim of this study is to assess an experimental approach for technological development of a direct compression formulation. A simple formula was considered composed by an active ingredient, a diluent and a lubricant. The active ingredient and diluent were selected as an example according to their typical densification mechanism: the nitrofurantoine, a fragmenting material, and the cellulose microcrystalline (Vivapur), which is a typical visco-elastic material, equally displaying good bind and disintegrant properties. For each ingredient, samples of different particle size distribution were selected. Initially, tabletability of pure materials was studied by a rotary press without magnesium stearate. Vivapur tabletability decreases with increase in particle size. The addition of magnesium stearate as lubricant decreases tabletability of Vivapur of greater particle size, while it kept unmodified that of Vivapur of lower particle size. Differences in tabletability can be related to differences in particle-particle interactions; for Vivapur of higher particle size (Vivapur 200, 102 and 101), the lower surface area develops lower surface available for bonds, while for Vivapur of lower particle size (99 and 105) the greater surface area allows high particle proximity favouring particle cohesivity. Nitrofurantoine shows great differences in compression behaviour according to its particle size distribution. Large crystals show poorer tabletability than fine crystals, further decreased by lubricant addition. The large crystals poor tabletability is due to their poor compactibility, in spite of high compressibility and plastic intrinsic deformability; in fact, in spite of the high densification tendency, the nature of the involved bonds is very weak. Nitrofurantoine samples were then mixed with Vivapurs in different proportions. Compression behaviour of binary mixes (tabletability and compressibility) was then evaluated according to diluents proportion in the mixes. The mix of either nitrofurantoine large crystals or fine crystals with cellulose microcrystalline showed a negative interaction in all proportions, whatever particle sizes. The lubricant addition induced a positive interaction with Vivapur of greater particle size distribution (200, 102 and 101) favouring higher particle adhesivity, while it maintained unaltered that of Vivapurs of lower particle size (105 and 99). Definitely, when cohesive forces are predominant (Vivapur 105 and 99), the establishment of adhesive bonds between nitrofurantoine and Vivapur remain unnoticed; on the contrary, when cohesion bonds between microcrystalline cellulose particles are weakened by the presence of magnesium stearate, the existence of adhesion bonds between particles of different nature is in evidence, leading to a positive interaction.

Compressive Strength↗
PubMed2004

Determination of tackiness of chitosan film-coated pellets exploiting minimum fluidization velocity.

The tackiness of aqueous chitosan film coatings and effects of anti-sticking agents on sticking tendency, were evaluated. A novel rapid method exploiting minimum fluidization velocity to determine tackiness was introduced and tested. The pressure difference over the miniaturized fluidized-bed was precisely recorded as a function of velocity of fluidization air. High molecular weight chitosan plasticized with glycerol was used as a film-forming agent. Magnesium stearate, titanium dioxide, colloidal silicon dioxide and glyceryl-1-monostearate (GMS) were studied as anti-sticking agents. Film coatings were performed in a miniaturized top-spray coater. The incorporation of anti-sticking agents led to a clear decrease in tackiness of the chitosan films, and magnesium stearate and GMS were shown the most effective. Film-coated pellets containing magnesium stearate and GMS as an anti-sticking agent were very easily fluidized (showing very low values of minimum fluidization velocity) and were thus classified as the best flowing and the least sticking samples. Both these additives were found anti-sticking agents of choice for aqueous chitosan film coatings. Determination of the experimental minimum fluidization velocity in a fluidized bed, is a useful and sensitive method of measuring the tackiness tendency of film-coated pellets.

Adhesiveness↗
PubMed1997

The high-affinity quinacrine binding site is located at a non-annular lipid domain of the nicotinic acetylcholine receptor.

This work deals with the localization of the high-affinity non-competitive quinacrine binding site on the muscle-type nicotinic acetylcholine receptor (AChR). Specifically, quantitative steady-state fluorescence spectroscopy is used to determine whether quinacrine binds to a site located at either the annular or the non-annular lipid domain. For this purpose, we measure the ability of spin-labelled phosphatidylcholine (SL-PC) to quench AChR-bound quinacrine, AChR-bound ethidium and membrane-partitioned 7-(9-anthroyloxy)stearate (7-AS) fluorescence. Additionally, we compare the accessibility of SL-PC which is considered to bind only to the annular lipid domain of the AChR with the accessibility of two non-annular domain-sensing lipids such as 5-doxylstearate (5-SAL) and spin-labelled androstane (ASL). Initial experiments using 7-AS established the experimental conditions for maximum SL-PC membrane partitioning. The non-specific quenching elicited by increasing turbidity of the sample after addition of SL-PC is corrected by means of parallel experiments with unlabelled egg yolk phosphatidylcholine. After correction, the SL-PC quenching experiments show the following order in quenching efficiency: 7-AS > quinacrine >> ethidium. The relative intrinsic sensitivity of quinacrine to TEMPO paramagnetic quenching in acetonitrile is considered to be approximately two times higher than that for 7-AS. Thus, SL-PC was found to be more accessible (about 5-fold) to the membrane-partitioned 7-AS than to the quinacrine locus. In addition, SL-PC was virtually not accessible to the high-affinity non-luminal binding site for ethidium. The relative capacity of SL-PC, 5-SAL, and ASL to quench AChR-bound quinacrine fluorescence indicated that the spin-labelled lipid accessibility to the quinacrine binding site follows the order: 5-SAL > ASL >> SL-PC. Examination of the effect of high concentrations of 5-SAL, of its unlabelled parent stearate, and of SL-PC on ethidium and quinacrine binding showed that: (a) both fatty acids displace quinacrine, but not ethidium, from its high-affinity binding site, however (b) 5-SAL was found to be more effective than stearate to displace quinacrine from its locus, whereas (c) SL-PC competes neither for the ethidium locus nor for the quinacrine binding site. The results suggest that the high-affinity binding site for quinacrine is located at a non-annular lipid domain of the AChR. This particular area has been considered to be located at the intramolecular interfaces of the five AChR subunits and/or at the interstices of the transmembrane domains.

Animals↗
PubMed2000

Novel sustained-release dosage forms of proteins using polyglycerol esters of fatty acids.

In order to develop a novel delivery system for proteins based on polyglycerol esters of fatty acids (PGEFs), we studied a model system using interferon-alpha (IFN-alpha) as the test protein. A cylindrical matrix was prepared by a heat extrusion technique using a lyophilized powder of the protein and 11 different types of synthetic PGEFs, which varied in degree of glycerol polymerization (di- and tetra-), chain length of fatty acids (myristate, palmitate and stearate) and degree of fatty acid esterification (mono-, di- and tri-). In an in-vitro release study using an enzyme-linked immunosorbent assay (ELISA) as a detection method, the matrices prepared from a monoglyceride (used for comparison) and from diglycerol esters exhibited a biphasic release pattern with a large initial burst followed by slow release. In contrast, the matrices prepared from tetraglycerol esters showed a steady rate of release without a large initial burst. In an in vivo release study, initial bursts of IFN-alpha release were, also, dramatically reduced when the matrices were prepared from the tetraglycerol esters of palmitate and stearate, and the mean residence time (MRT) of IFN-alpha was prolonged, whereas the matrices prepared from monoglyceride and from diglycerol esters showed large initial bursts of IFN-alpha release. Since the release rates from the matrices prepared from the tetraglycerol esters of palmitate and stearate were governed by Jander's equation modified for a cylindrical matrix, the release from those matrices was concluded to be a diffusion-controlled process. The bioavailability of IFN-alpha after implantation of the matrix formulation prepared using all types of PGEFs, except for tetraglycerol triesters, was almost equivalent to that after injection of IFN-alpha solution; consequently, IFN-alpha in these matrices appears to remain stable during the release period.

Animals↗
PubMed1984

Comedogenicity of current therapeutic products, cosmetics, and ingredients in the rabbit ear.

Cosmetics continue to be used by acne-prone individuals. Often as more acne develops, more cosmetics are applied. In order to protect against this natural tendency, physicians should provide more patient information on the currently available products and ingredients. This presentation is designed to help in that effort. The data presented were gleaned from the rabbit ear assay, which is not an ideal animal model but is the best we have. If an ingredient is negative in the rabbit ear assay, we feel it is safe on the acne-prone skin. A strong, positive ingredient or cosmetic should be avoided. Ingredient offenders include isopropyl myristate and its analogs, such as isopropyl palmitate, isopropyl isostearate, butyl stearate, isostearyl neopentanoate, myristyl myristate, decyl oleate, octyl stearate, octyl palmitate or isocetyl stearate, and new introductions by the cosmetic industry, such as propylene glycol-2 (PPG-2) myristyl propionate. Lanolins continue to be a problem, especially derivatives such as acetylated or ethoxylated lanolins. Our most troublesome recent finding is the comedogenic potential of the D & C Red dyes. They are universally used in the cosmetic industry, especially in blushers. This may explain the predominance of cosmetic acne in the cheekbone area. All of these D & C Red dyes tested to date, the xanthenes, monoazoanilines, fluorans, and indigoids, are comedogenic. Actually, this is not surprising as they are coal tar derivatives. The natural red pigment, carmine, is noncomedogenic and can serve as a substitute for D & C dyes in blushers. Many finished products are comedogenic. Most troublesome to the dermatologists are the therapeutic tools that we use, such as Liquimat, Retin-A cream, Hytone, Staticin, Sulfoxl, Desquam-X, and Persadox HP cream. These should be reformulated. We have been unable to confirm that precipitated sulfur (U.S.P.) is a potent comedogen in the rabbit ear assay. Clinically, we still find sulfur quite effective as an adjuvant to the benzoyl peroxide therapy for the treatment of acne vulgaris. We would suggest that the bias against sulfur be reconsidered.

Acne Vulgaris↗
PubMed2003

Further investigations into the use of high sensitivity differential scanning calorimetry as a means of predicting drug-excipient interactions.

The early prediction of drug-excipient incompatibility is vital in the pharmaceutical industry to avoid costly material wastage and time delays. We report here on the use of high sensitivity differential scanning calorimetry (HSDSC) to examine the compatibility between an experimental drug (Drug A) and common pharmaceutical excipients. Short-term HSDSC experiments (up to 25h) indicated that Drug A was stable in the presence of moisture and was compatible with both lactose monohydrate and magnesium stearate in the dry state, but showed degradation in the presence of magnesium stearate and water in combination. These results agreed with conventional stability studies, in which extensive degradation was observed in the Drug A-magnesium stearate system after storage at 40 degrees C/75% RH for 4 weeks but not under other conditions. These results indicate that HSDSC may be used to examine the compatibility of experimental drugs with conventional excipients and, in particular, illustrate the importance of incorporating humidity as an experimental variable in order to fully establish the stability profile of the material under test.

Calorimetry, Differential Scanning↗