This may imply that ligands for these receptor subtypes are non-selective buy zoloft online pills depression screening test, such as the adenosine receptor antagonists caffeine and theophylline buy zoloft with american express bipolar depression symptoms in women. Additionally purchase zoloft with american express depression of 1837, receptor selectivity may vary with relatively small changes in ligand structure: an 8-cycloalkyl substituent on theophylline confers A1 receptor selectivity, whereas a phenylstyryl substituent on the same position in caffeine renders these compounds selective for the A2A receptor. The purinergic receptor P2Y12 is found near the adenosine receptors owing to the purine core typical for ligands of both these subfamilies. In agreement with the ligand selectivity reported for the α1-, α2-, and β-adrenoceptor subfamilies, these receptors form three distinct 26 clusters; furthermore, the α1B and α1D receptors are the closest in the distance matrix. This indicates the presence of distinct chemical classes in the ligand set of the M2 receptor, which may be the result of inclusion of allosteric ligands. In general, the remaining aminergic receptors (serotonergic, dopaminergic, histaminergic and cholinergic) are more scattered throughout the substructure tree. The grouping of the eight prostanoid receptors (Figure 2) indicates similarity in substructure profiles of the ligands. This is based on the fact that 35, 36 most prostanoid receptor ligands are direct derivatives of the endogenous ligands, the so-called eicosanoids. These ligands are highly similar, all consisting of large aliphatic, lipophilic alkyl chains. The presence of the leukotriene and cannabinoid receptors in this lipid cluster may seem strange at first. Leukotrienes are however also eicosanoids, which clarifies the position of the leukotriene B4 and cysteinyl-leukotriene 37, 38 receptors in this cluster. In addition, arachidonic acid is the common precursor for eicosanoids and two derivatives of arachidonic acid, anandamide and 2- arachidonylglycerol, both of which are endogenous ligands (‘endocannabinoids’) of the cannabinoid receptors. The relationship between target clustering in the substructure tree (Figure 2) and ligand promiscuity suggests that the substructure tree may be used to identify possible side effects on receptors that are close neighbors in this tree. If inspection reveals a ligand to bind to receptor(s) that are phylogenetically related to the target of interest, a more detailed experimental follow-up with respect to receptor selectivity would be worthwhile. For instance, with the exclusion of the glycoprotein, P2Y, angiotensin, and bradykinin receptors, all other receptors represented by two subtypes occur in pairs in both the ligand tree and the sequence tree. In addition, the prostanoid receptors largely group together in both trees, as do most of the aminergic receptors. D1 and D5 (D1-like) versus D2, D3, and D4 (D2-like), exists both in the sequence-based classification and 39 ligand-based classification. This is in agreement with a previous study and also known from drugs on the market such as the benzazepines that favor D1–like over D2-like dopamine receptors. Similarly, antipsychotics such as chlorpromazine have a higher 40 affinity for the D2-like subtypes than D1-like receptors. The fact that many clusters arise in both trees indicates that the receptors in these clusters have similar sequences and similar ligands, that is, ligands with substantially overlapping substructure sets. The (qualitative) similarities and differences among sequence and substructure trees are discussed in the following. This plot, provided in Figure 3 (and described in detail in the Materials and Methods section), visualizes how receptor distances deviate between the sequence-based tree and the ligand-based classification of receptors. In sequence space, receptor distances indicate the (dis)similarly between protein sequences, while in ligand space, receptor distances reflect the overlap in structural features found in ligands for these receptors. From the delta-delta plot, it becomes apparent that the prostanoid receptors and P2Y1 receptor are on average the most distant receptors from the rest of the classes. This may be a reflection of the evolutionary relationship between sequences, which results in coverage of a small region of the overall sequence space. The ligands for these targets do not have such a direct relationship and thus cover a broader range in overall substructure space. The difference between ligand-based and target-based classifications may be due to 43 convergent evolution. Functional convergence denotes how proteins that differ in sequence may fulfill the same protein function. These may therefore have a different selectivity profile compared to the endogenous ligand. Delta-delta plot visualization of receptor distances in sequence and substructure space. The average distance towards the other targets is plotted for sequence and substructure space. Targets that are, on average, more distant from the rest are plotted further away from the origin; targets plotted above the diagonal are more distant in sequence space, while targets plotted below the diagonal are more distant in substructure space. This indicates that this receptor is, in general, more distant from the other receptors, most prominent in sequence space. Example plots expressing the performance of the simulated receptor de-orphanization. The full set of plotted scores is provided in Additional file 2 – Plotted scores for the leave-one-out validation. For each plot, receptors are ordered along the x-axis (labeled “Number of included receptors”) in order of increasing distance in sequence space to the receptor under study. On the y-axis (labeled “Ligands identified”), the cumulative number of retrieved ligands is depicted, normalized linearly to the interval [0;1]. The red curve indicates the number of active ligands that are retrieved when including all (closest) receptors that are listed along the x-axis up to that point. The blue diagonal illustrates recovery of ligands when performance is equal to random prediction. For each receptor in the dataset, we pretended not to know any of its ligands by excluding them from the datasets (we ‘orphanized’ the receptor in this particular run of the protocol). We next predicted its ligands by considering a model derived from the closest neighbors of the receptor in sequence space (we attempted to ‘de-orphanize’ the receptor whose ligands we omitted from the study in the previous step). The cumulative number of correctly identified ligands of every receptor is plotted against the number of closest neighbors (sequences) included to find these ligands. Curves of the second category display a gradual rise that is approximately equal to the diagonal of the plot. The steep rises are caused by a few receptors identifying the majority of ligands. The poor performance concerning the P2Y1 receptor is probably due to the nature of its ligands: this set consists of a small number of highly similar ligands that all possess a phosphate group, a feature not found in other ligands in the database. The number of features (substructures) shared with ligands of this receptor and other receptors is therefore small. Interestingly, the adenosine A1 and A3 receptors, which are also purinergic, identify most (28 out of 42) of the P2Y1 ligands. However, in sequence space these receptors are at great distance (at positions 91 and 92, respectively). The absence of a receptor may influence the order of other receptors in the trees.

How cholinergic drugs work Cholinergic drugs fall into one of two major classes: cholinergic agonists and anticholinesterase drugs discount 50mg zoloft free shipping depression inventory test. Cholinergic agonists Anticholinesterase drugs When a neuron in the parasympathetic nervous system is stim- After acetylcholine stimulates the cholinergic receptor 50 mg zoloft visa depression symptoms questions, it’s de- ulated discount zoloft american express depression meds, the neurotransmitter acetylcholine is released. Anticholinester- choline crosses the synapse and interacts with receptors in an ase drugs inhibit acetylcholinesterase. Cholinergic agonists stimulate cholinergic re- line isn’t broken down and begins to accumulate, leading to ceptors, mimicking the action of acetylcholine. Pharmacokinetics (how drugs circulate) The action and metabolism of cholinergic agonists vary widely and depend on the affinity of the individual drug for muscarinic or nicotinic receptors. Metabolism and excretion All cholinergic agonists are metabolized by cholinesterases: • at the muscarinic and nicotinic receptor sites • in the plasma (the liquid portion of the blood) • in the liver. Pharmacodynamics (how drugs act) Cholinergic agonists work by mimicking the action of acetylcho- line on the neurons in certain organs of the body called target or- gans. Examples include the following: • Other cholinergic drugs, particularly anticholinesterase drugs (such as ambenonium, edrophonium, neostigmine, physostigmine, Adverse and pyridostigmine), boost the effects of cholinergic agonists and reactions to increase the risk of toxicity. Because they bind with • Quinidine also reduces the effectiveness of cholinergic agonists. As acetylcholine builds up, it continues to stimu- fects can include: late the cholinergic receptors. One day at a time: Recognizing a toxic response It’s difficult to predict adverse reactions to an- Enter edrophonium ticholinesterase drugs in a patient with myas- Deciding whether a patient is experiencing a thenia gravis because the therapeutic dose toxic drug response (too much drug) or a my- varies from day to day. Increased muscle asthenic crisis (extreme muscle weakness and weakness can result from: severe respiratory difficulties) can be difficult. When edrophonium is used, suction, oxygen, mechanical ventilation, and emer- gency drugs, such as atropine, must be readily available in case a cholinergic crisis occurs. Pharmacokinetics Here’s a brief rundown of how anticholinesterase drugs move through the body. Because the duration of action for an oral dose is longer, however, the pa- tient doesn’t need to take it as frequently. Distribution Physostigmine can cross the blood-brain barrier (a protective bar- rier between the capillaries and brain tissue that prevents harmful substances from entering the brain). Donepezil is highly bound to plasma proteins, tacrine is about 55% bound, rivastigmine is 40% bound, and galantamine is 18% bound. Depending on the dosage, anticholinesterase Pharmacodynamics drugs can produce a Anticholinesterase drugs promote the action of acetylcholine at stimulant or receptor sites. From minutes to weeks Reversible anticholinesterase drugs block the breakdown of acetylcholine for minutes to hours; irreversible anti- cholinesterase drugs do so for days or weeks. Drug interactions These interactions can occur with anticholinesterase drugs: • Other cholinergic drugs, particularly cholinergic agonists (such as bethanechol, carbachol, and pilocarpine), increase the risk of a toxic reaction when taken with anticholinesterase drugs. Most of the adverse re- actions caused by anti- cholinesterase drugs re- Cholinergic blocking drugs sult from increased ac- tion of acetylcholine at Cholinergic blocking drugs interrupt parasympathetic nerve im- receptor sites. These drugs Adverse reactions are also referred to as anticholinergic drugs because they prevent acetylcholine from stimulating cholinergic receptors. Muscarinic receptors are • diarrhea cholinergic receptors that are stimulated by the alkaloid mus- • shortness of breath, carine and blocked by atropine. Next come their synthetic sisters Synthetic derivatives of these drugs (the quaternary ammonium drugs) include: • glycopyrrolate • propantheline. Atropine may also be used as an antidote for nerve agents (See the appendix, Vaccines and antidotes for biological and chemical weapons. Distribution The belladonna alkaloids are distributed more widely throughout the body than the quaternary ammonium derivatives or dicyclo- mine. The alkaloids readily cross the blood-brain barrier; the other cholinergic blockers don’t. Metabolism and excretion The belladonna alkaloids are only slightly to moderately protein- bound. This means that a moderate to high amount of the drug is active and available to produce a therapeutic response. The bel- ladonna alkaloids are metabolized in the liver and excreted by the kidneys as unchanged drug and metabolites. Pharmacodynamics Cholinergic blockers can have paradoxical effects on the body, de- pending on the dosage and the condition being treated. Dual duty Cholinergic blockers can produce a stimulating or depressing ef- fect, depending on the target organ. In the brain, they do both— low drug levels stimulate, and high drug levels depress. Conditional considerations The effects of a drug on your patient are also determined by the patient’s disorder. Parkinson’s disease, for example, is character- ized by low dopamine levels that intensify the stimulating effects of acetylcholine. The quaternary ammo- nium and amine compounds such as propantheline are the drugs of choice for these conditions because they cause fewer adverse reactions than belladonna alkaloids. Before surgery Cholinergic blockers such as atropine are given before surgery to: • reduce oral, gastric, and respiratory secretions • prevent a drop in heart rate caused by vagal nerve stimulation during anesthesia. How atropine speeds the heart rate To understand how atropine affects the heart, first consider inhibits electrical conduction and causes the heart rate to slow how the heart’s electrical conduction system functions. Atropine is the drug of choice to treat: • symptomatic sinus bradycardia—when the heart beats too slow- ly, causing low blood pressure or dizziness (see How atropine speeds the heart rate) • arrhythmias resulting from the use of anesthetics, choline es- ters, or succinylcholine. That means that they: • paralyze the ciliary muscles of the eye (used for fine focusing) • alter the shape of the eye lens. Moreover, cholinergic blockers act as mydriatics to dilate the pupils, making it easier to measure refractive errors during an eye examination or to perform eye surgery. Punishing pesticides The belladonna alkaloids, particularly atropine and hyoscyamine, are effective antidotes to cholinergic and anticholinesterase drugs. Atropine is the drug of choice to treat poisoning from organophosphate pesticides. Atropine and hyoscyamine also counteract the effects of the neuromuscular blocking drugs by competing for the same receptor sites. This increases the amount of the drug that’s absorbed and, therefore, increases the risk of ad- verse effects. Increased effect… Drugs that increase the effects of cholinergic blockers include: • disopyramide • antidyskinetics such as amantadine • antiemetics and antivertigo drugs, such as buclizine, cyclizine, meclizine, and diphenhydramine • antipsychotics, such as haloperidol, phenothiazines, and thio- xanthenes • cyclobenzaprine • orphenadrine • tricyclic and tetracyclic antidepressants. Mixing it up some more Other drug interactions can occur: • The risk of digoxin toxicity increases when digoxin is taken with a cholinergic blocker. With these drugs, the Adrenergic drugs are classified into two groups based on their difference between a chemical structure—catecholamines (naturally occurring as well therapeutic dose and a as synthetic) and noncatecholamines. They can be: may include: • direct-acting, in which the drug acts directly on the organ or tis- • dry mouth sue innervated (supplied with nerves or nerve impulses) by the • reduced bronchial se- sympathetic nervous system cretions • indirect-acting, in which the drug triggers the release of a neu- • increased heart rate rotransmitter, usually norepinephrine • decreased sweating.

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In other words generic zoloft 100 mg with mastercard endogenous depression definition psychology, the accuracy and significance of measurements may be solely limited by the sampling process cheap 50mg zoloft depression rates by state. Unless and until the sampling process is performed properly buy discount zoloft 50mg online depression elevation definition, it may give rise to a possible weak link in the interpretation of the analytical results. However, a good deal of the wisdom of the analyst supported by the application of statisical results and wealth of experience may go a long way in achieving reasonably accurate and reproducible results. Sampling Procedures Samples may be categorized broadly into four heads, namely : (a) Gross Sample : A sample that represents the whole lot and may vary from a few grams or less to several pounds based on the nature of the bulk material. For Solids Sampling of solid materials are comparatively more difficult than other materials because of the follow- ing three reasons, namely : (a) Variation in particle size. Sampling of solids can be best accomplished by adopting the following procedures : • To take 1/50 to 1/100th of the total bulk for gross samples. For Liquids Sampling of liquids may be carried out by following these procedures : • Small heterogenous liquid samples are first shaken thoroughly and then followed by immediate sampling. However, the latter method is preferred for obvious reasons since the analysis shall have a better hold on the accuracy and precision of the analysis. A few specific examples are stated below : (a) A 24 hour urine sample collections are usually more reliable than single specimens. For example : (a) A breathe sample may be collected by allowing the subject to blow into an evacuated bag. Errors The famous adage—‘to err is human to forgive divine’—literally means that it is natural for people to make mistakes. However, errors in analytical chemistry or more precisely in pharmaceutical drug analysis are normally of three types, namely : (a) Determinate Errors (b) Instrumental Errors (c) Personal Errors These above mentioned errors would be discussed briefly here with specific examples. It is pertinent to mention here that errors outside the range of ‘permissible errors’ in the analyses of pharmaceutical substances may cause serious problems because most of these substances are usually highly toxic, potent and used exten- sively in life-saving processes across the globe. Determinate Errors Errors caused due to either incorrect adoption of an assay method or an incorrect graduation read out by an analyst are termed as determinate errors. In usual practice the determinate errors are subtle in nature and hence, not easily detected. A few typical examples of determinate errors are stated below : (a) Gravimetric Analysis : Where a compound is precipitated from a solution and the analyst believes that the analyte has been removed from the solution completely. Actually a small portion of the substance under investigation shall remain in solution. It may require an excess quantity of reagent to affect the colour change which ultimately shows completion of the chemical reaction between reagent and analyte. Therefore, in all such analytical procedures a ‘blank titration’ is performed simultaneously to determine how much reagent is required to affect the colour change when no analyte is present. Instrumnetal Errors The past three decades have witnessed a quantum progress and advancement in the field of analytical chemistry. Nowadays, both microprocessor based and computer-aided analytical instruments have more or less replaced the manually operated ones in any reasonably good analytical laboratory. One of the most prevalent determinate errors is caused by analytical intruments which are found to be ‘out of calibration’. Hence, it is very essential that such instruments need to be calibrated periodically, for instance, a pH meter is calibrated using a buffer solution of known pH, say adjusting the meter to read pH = 7. Personal Errors In addition to errors caused due to improper assay methods or faulty instruments, it may also be due to the analyst. A few typical examples are cited below : (a) Physical Impairment : A person suffering from colour blindness may not be in a position to assess colour-changes precisely ; or if he uses bifocals he may not take the burette readings accurately. Importance There are three major factors that govern the efficacy of a dosage form, namely : (a) Onset of therapeutic activity. The above three factors are solely responsible for the rate of absorption of the drug, the distribution of the drug throughout the circulatory system and above all the elimination of the active principle from the body. Moreover, even the products of the same manufacturer may have varying degree of bioavailability in different batches. Therefore, it has become quite necessary to introduce comparative bioavailability studies and skillfully designed fool-proof clinical tests of therapeutic equivalence as an effective true remedial measure of the ultimate performance of drug products. In 1968, fifty-one patients suffered from an epidemic of anticonvulsant intoxication in Brisbane. A thorough investigation revealed that the intoxication was caused by altering one of the excipients from calcium phosphate to lactose in the drug product Phenytoin Capsule without adequate pre-testing by the manufacturer. Question of Quality It has now been established beyond any reasonable doubt that quality of a drug product cannot simply be ensured by inspection or analysis, but a control system has to be built into, from the very beginning of manufac- ture of a drug. Besides effective quality control measures exercised in every aspects of production including environment, screening of raw materials, process controls, intermediate shelf-life of finished products the most important aspect is to assess the bioavailability of the active principle. Difference in bioavailability, particularly in drugs with low solubilty, as ascertained by blood level attainment studies, appears to be caused by a number of formulation variables, namely : particlesize, crystalline structure, binding or disintegrating agent, excipient etc. For example : the rate of dissolution of the drug in tablet or a capsule in the gastrointestinal fluids. Clinical Efficacy of Drugs Medical scientists mainly rely on the measurement of bioavailability of a drug as a positive indicator of therapeutic equivalence, because clinical efficacy for orally administered drugs depends on the degree of absorption and the presence of the active ingredient in the blood stream. Technical information based on in vivo standards and specifications are generally incorporated in vari- ous official compendia. Hence, in order to record a legitimate assessment of bioavailability, in vivo test is an absolute necessity and the relative data obtained therefrom should form an integral part of the standard specifi- cations in the offcial standard. Hence, a regular feed back of relevant informa- tion on such adverse reactions from the medical practitioners to the appropriate regulatory authorities and the concerned manufacturers would not only help to intensify better safety measures but also widen the scope to improve drug-design by meticulous research scientists all over the world. They are : Example 1 : Aspirin—Increased gastric damage and subsequent bleeding caused by some aspirin fomulations have been specifically attributed to the slowly dissolving aspirin particles in the stomach. However, both effervescent and highly buffered dosage forms (antacid-aspirin-tablet), which help in maintaining the aspirin in solution, have been found to minimise gastro-intestinal toxicity. The physical constants essentially include the melting point, boiling point, refractive index, weight per millilitre, specific optical rotation, light absorption, viscosity, specific surface area, swelling power, infra-red absorption, and the like. However, the most specific and reliable are the chemical tests which may be categorized separately under tests for inorganic substances and organic substances. The former may be carried out by well defined general quantitative inorganic analysis and the latter by specific reactions of one or more of the functional moieties present in a drug molecule. These physical constants will be discussed briefly with typical examples as under : 1. Melting Point It is an important criterion to know the purity of a substance ; however, it has a few limitations. The accuracy and precision of melting point is dependent on a number of factors such as—capillary size, sample size, initial temperature of heating-block and the rate of rise of temperature per unit time (minutes). Keeping in view the different manufacturing processes available for a particular drug the melting point has a definite range usually known as the melting range. Mestranol 146 154 Thus the melting range takes care of the variance in manufacture together with the storage variance over a stipulated period of time. Boiling Point It is also an important parameter that establishes the purity of a substance.

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Formulations of Semisolid Drugs 161 Foscarnet Cream Bill of Materials Scale (mg/100 g) Item Material Name Quantity/kg (mg) 3 zoloft 25 mg free shipping depression live chat. Melt items 2 buy generic zoloft canada depression part 2, 3 purchase zoloft 50 mg amex anxiety management, and 5 at 70°C in a small con- step 2 to the step 3 while stirring. Transfer the ointment to stainless steel drum filter to mixer and cool it down to 50°C. Formulations of Semisolid Drugs 163 Gentamicin Sulfate Cream Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 0. Quantity of gentamicin sulfate per batch will vary according to the actual potency. While homogenization is in progress, set the steel filter while mixing at speed 10 rpm, vac- temperature at 25°C so that the cream temper- uum 0. Stop the homogenizer, set the mixer at temper- cream in stainless steel container and fill. Gentamicin Sulfate Ointment Gentamicin sulfate ointment is a sterile, topical anti-infective (equivalent to 3. Gentamicin sulfate is the sulfate salt of gentamicin tamicin sulfate equivalent to 0. Immediately The suppository mass is manufactured at a temperature of transfer the hot mass to the heated storage ves- 120°C. Care must be taken to see that molten suppository sel or heated vessel of suppository filling mass does not accidentally spill on the person. Glycerin Suppositories Bill of Materials Scale (mg/suppository) Item Material Name Quantity/1000 Suppositories (g) 900. Formulations of Semisolid Drugs 165 Glycolic Acid Cream Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 3. Gramicidin, Neomycin, Nystatin, and Triamcinolone Ointment Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 0. Rinse homogenizer with liquid paraffin and add heat to 70°C to melt; transfer to Becomix rinsings. Mix till ointment is smooth, transfer to a stain- twice with fine-gap setting to make smooth dis- less steel vessel, and fill. Charge items 1, 2 (balance quantity), 3, and 6 in a separate stainless steel vessel and homogenize 166 Handbook of Pharmaceutical Manufacturing Formulations: Semisolid Products Halobetasol Propionate Cream and Ointment The cream contains halobetasol propionate, a synthetic halobetasol propionate in a cream base of cetyl alcohol, corticosteroid for topical dermatological use. The corti- glycerin, isopropyl isostearate, isopropyl palmitate, ste- costeroids constitute a class of primarily synthetic steroids areth-21, diazolidinyl urea, methylchloroisothiazolinone, used topically as an anti-inflammatory and antipruritic methylisothiazolinone, and water. Heparin Gel-Cream Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 0. Formulations of Semisolid Drugs 167 Hexachlorophen Cream Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 45. While both solutions are at 65°–70°C, form the primary emulsion by pumping the aqueous solu- 1. Strain olive oil through voile cloth or equivalent tion from step 5 into the oil mixture from step 3 into a suitable stainless steel-jacketed tank. Homogenize primary emulsion through a Troy ate mix, add cetyl alcohol, lanolin, petrolatum, Mill, or similar device, into the balance of aque- and polysorbate 40 with mixing. Add and dissolve hexachlorophene in the oil emulsion should strained through voile cloth or mix, then add and disperse the simethicone. Cool emulsion to 40°–50°C with agitation glycerin, methylparaben, and borax as purified under vacuum. Reserve 4 mL of solution from step 5 in a separate container to rinse equipment in step 2. Other formulations include base containing sorbitan sesquioleate, water, aquaphor, cream, which contains hydrocortisone acetate 1% or 2. Hydrocortisone Ointment Bill of Materials Scale (mg/100 g) Item Material Name Quantity/kg (g) 1. In a separate vessel, disperse item 1 in item 3, using a spatula, in a water bath maintained at 60°C. Hydrocortisone Acetate Suppositories Hydrocortisone acetate is a corticosteroid designated blended hydrogenated vegetable oil base. Dissolve item 2 in balance of item 9 and a vessel after passing through stainless steel sieve portion of item 5 in a separate vessel and and heat to melt. Hydrocortisone Butyrate Cream and Ointment The cream, ointment, and topical solution contain the base consisting of cetostearyl alcohol, ceteth-20, mineral topical corticosteroid hydrocortisone butyrate, a nonflu- oil, white petrolatum, citric acid, sodium citrate, propylpa- orinated hydrocortisone ester. It has the chemical name raben and butylparaben (preservatives), and purified water. Transfer the oil phase to the aqueous phase in a mixer vessel through mesh by vacuum while stirring at manual mode, 10 rpm, temperature 60°C. Formulations of Semisolid Drugs 171 Hydrocortisone Cream Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 70. Heat items 7 and 8 until the active ingredient is dissolved, mix with 1/2, and continue to stir 1. Hydrocortisone Cream Bill of Materials Scale (mg/100 g) Item Material Name Quantity/kg (g) 1. Transfer the oil phase from step 2 into step 5 through vacuum transfer while stirring at man- 1. Load items 4–7 in a fat-melting vessel (the oily ual 10 rpm and temperature of 60°C. Cool down to 30°C while mixing at 10 rpm auto dissolve by mixing for 10–15 minutes at mode and under vacuum of 0. Another formulation of cream with aloe ferent types of itches and rashes; it is available in 1% and contains the active ingredient hydrocortisone 1%, and the 0. For 1% cream, the inactive ingredients are inactive ingredients aloe barbadensis gel, aluminum sul- aloe vera, benzyl alcohol, ceteareth-20, cetearyl alcohol, fate, calcium acetate, cetearyl alcohol, glycerin, light min- cetyl palmitate, glycerin, isopropyl myristate, isostearyl eral oil, maltodextrin, methylparaben, potato dextrin, pro- neopentanoate, methylparaben, and purified water. For the pylparaben, purified water, sodium cetearyl sulfate, 1% ointment, they are butylparaben, cholesterol, meth- sodium lauryl sulfate, white petrolatum, and white wax. The intensive therapy cream includes cetyl fate, calcium acetate, cetearyl alcohol, glycerin, light min- alcohol, citric acid, glyceryl stearate, isopropyl myristate, eral oil, maltodextrin, methylparaben, potato dextrin, pro- methylparaben, polyoxyl 40 stearate, polysorbate 60, pro- pylparaben, purified water, sodium cetearyl sulfate, pylene glycol, propylparaben, purified water, sodium cit- sodium lauryl sulfate, white petrolatum, and white wax. Formulations of Semisolid Drugs 173 Hydrocortisone Gel Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 10. Prepare solution of item 4, heat item 5 to 70°C and add slowly to the hot-mixture item 4. Hydrocortisone Gel Bill of Materials Scale (mg/g) Item Material Name Quantity/kg (g) 5. Hydrogen Peroxide Ointment Bill of Materials Scale (g/100 g) Item Material Name Quantity/kg (g) 5. Add methylparaben and mix the composition at 61°–65°C, draw the oil phase into the to dissolve while maintaining temperature. While mixing and under vacuum, allow the monostearate, and white beeswax and mix mixture to cool gradually to room temperature. Melt the stearyl alcohol and the white petrola- tum on a steam bath and warm to about 75°C. Hydroquinone is struc- In another formulation, the each gram of 4% cream turally related to monobenzone.