1.

1 General Introduction

Two decades ago, the remedy for hypercholesterolemia and high blood pressure was predicted to
remove cardiovascular disease (CVD) with the advent of the 20th century. Recently, however,
that positive prediction has wanted revision. Cardiovascular ailments are predicted to be the
predominant cause of death globally within the subsequent 15 years owing to a rapidly growing
incidence in developing nations and Eastern Europe and the rising prevalence of weight
problems and diabetes in the Western world [Goran,2005]. Around less than 18 million
individuals passed on from CVDs in 2017. The more significant part (64 percent) of passing’s
happened in the age section of 70 years or more. Just underneath 30 percent were matured 50-69,
and the remaining grow 15-49 (CVD passing's in those aged 14 years and under are little). In
Bangladesh, age-institutionalized passing rates from cardiovascular sickness are 298 estimated as
the number of deaths per 100,000 people crosswise over both genders [Hannah & Max,2019].
Cardiovascular maladies include the cardiovascular framework: heart, veins, and the circulatory
framework. They represent the primary reason behind illogicality in developed countries
[Moor,2017].

When there is a development of cholesterol plaque in the artery partitions, then coronary artery
disease occurs. Raised levels of blood lipids are well-recorded hazard factors for cardiovascular
ailment. Present day essential care specialists spend significant time and exertion on preventative
medication. Diagnosing and overseeing hyperlipidemia as an approach to forestall cardiovascular
disease (CVD) is a normal movement for essential care doctors. As per the Centers for Disease
Control statistics from a study of 1,492 medical practitioners who provides ambulatory care in
non-government settings, hyperlipidemia is second only to hypertension in the list of the ten
most common persistent stipulations. The truth that hyperlipidemia is a robust risk component
for CVD appropriately established. Hyperlipidemia alludes to raised cholesterol, raised TG, or
both [Nelson,2012]. Cholesterol is fundamental for the working of every human organ, but it's
far though the reason for coronary heart sickness. Coronary artery disease (CAD) is an
undeniably significant restorative and general medical issue and is the primary source of
mortality in Bangladesh. Like other South Asians, Bangladeshis are unduly inclined to create
CAD, which is untimely in the beginning, pursues a quickly dynamic course and
angiographically greater extreme [Islam & Majumder,2013].

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Through the span of almost an era of examination, researchers have built up a few lines of proof
establish that the causal association between blood cholesterol, atherosclerosis, and coronary

illness. Expanding on that information, researchers and the pharmaceutical companies have
effectively built up a strikingly powerful class of medications, the statins that lower cholesterol
levels in the blood and diminish the recurrence of heart assaults [Beppu,2010].

There may be proof to propose that statin treatment is related to a factually critical decrease in
the danger of essential and auxiliary cardiovascular diseases [Ward et al, 2007]. Statins are a
trustworthy and well-endured class of lipid-modifying drugs that have been appeared to diminish
the threat of starting and common cardiovascular diseases. Nevertheless, cerivastatin returned
from the world market, given its potential for severe myotonic impacts. Since the advantages of
statin treatment exceed the little danger of side effects, statins remain the primary line treatment
for lipid-lowering drug down and confining atherosclerotic cardiovascular diseases
[Rosenson,2004]. For the avoidance of cardiovascular infection caused because of
hypercholesterolemia, at present, seven affirmed statins; atorvastatin, fluvastatin, lovastatin,
pitavastatin, pravastatin, rosuvastatin, and simvastatin broadly utilize. Patients treated in a typical
consideration setting with rosuvastatin fundamentally more noteworthy decreases in LDL
cholesterol, non-HDL cholesterol, and overall cholesterol levels in contrast to those obtained
from atorvastatin [Michael.2007].

1.2 Statins

The statins are a broadly utilized class of cholesterol-lowering agents that work by blocking the
enzyme 3-hydroxy 3-methyl glutaryl CoA (HMG CoA) reductase, which catalyses the rate-
restricting step in cholesterol biosynthesis [Armitage et al., 2007]. Since statins first affirmed in
1987, their capacity to decrease the dangers of vascular passing, non-lethal myocardial localized
necrosis, stroke, and the requirement for blood vessel revascularization
methods have appeared to be a few enormous and high calibre randomized preliminaries. 

Cholesterol-lowering is presently suggested for a broad group of individuals at cardiovascular

hazard, incorporating those with normal and below normal lipid levels. This change is assisting
the expanded statin use and to the utilization of progressively escalated regimens. Subsequently,
the security of this group of medications has profound significance. 

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Collectively there are seven statins accessible in many places of the world, for example,
lovastatin (first authorized in 1987), simvastatin (1988), pravastatin (1991), fluvastatin (1994),
atorvastatin (1997), rosuvastatin (2003), and pitavastatin (2003-accessible in Japan and India
only). Cerivastatin was endorsed in 1998; however, then it was pulled back in 2001 because
of the excessive danger of rhabdomyolysis.

1.3 Rosuvastatin: A New Drug

Almost for two decades, it has been proved that there has sensational decrease in cardiovascular
hazard utilizing 3-hydroxy-3-methyl glutaryl coenzyme A reductase inhibitors ("statins") to
lower levels of low-density lipoprotein (LDL) cholesterol [Shuhaili et al., 2017].When all said in
done, a 21% decrease in the danger of major cardiovascular events is related with each 1 mmol/L
(39 mg/dL) decline in LDL cholesterol. In any case, regardless of this remedial achievement, the
lingering danger of major cardiovascular events stays high. Rosuvastatin is the premise of logical
and general wellbeing enthusiasm for new medications, and intercession methodologies went for
diminishing the still high cardiovascular hazard in the populace. 

Like other statins, rosuvastatin is a synthetic statin that shows a development in the
pharmacologic and clinical characteristics of statins. Relative to other statins, rosuvastatin
possesses a higher number of binding interactions with HMG-CoA reductase and has a huge
attraction for the active area of the enzyme. In hepatic cells, rosuvastatin is comparatively water-
soluble and correctly taken up by cells. Among statins, rosuvastatin has the prolonged end-stage
half-life and is just negligibly metabolized by the cytochrome P450 (CYP 450) enzyme
system. The prediction with this finding is the non-appearance of clinically noteworthy drug
interactions between rosuvastatin, and different drugs are repressing CYP 450 enzymes. The
impacts of statins on lipid profiles are dose-dependent. Hence, investigations demonstrated that
rosuvastatin has the best effect on the lipid profile.

1.4 Development History of Rosuvastatin

April 1998

AstraZeneca reported that it had authorized overall privileges of a compound it named

rosuvastatin from Shinogi and Co. of Japan.

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July 31, 2000

Only eight months after permitting the item from Shinogi and Co., AstraZeneca reported that it
had finished the whole Western Phase I and II clinical preliminaries, accepted to be a record time
for an essential care product.

June 27, 2001

AstraZeneca reported that a New Drug Application for CRESTOR (Rosuvastatin) submitted to
the U.S. FDA and European specialists for the management of hypercholesterolemia, mixed
dyslipidemia, and isolated hypertriglyceridemia.

November 7, 2002

AstraZeneca declared it had gotten the primary endorsement for CRESTOR (Rosuvastatin) in
Netherlands for the administration of essential hypercholesterolemia and blended dyslipidemia.

In this case, the Netherlands is about to go as the Reference Member State for the European
Mutual Recognition Procedure prompting endorsements in 16 different nations in Europe.

August 13, 2003

AstraZeneca declared that its new cholesterol-lowering the drug and CRESTOR (Rosuvastatin)
got an endorsement from the U.S. FDA, as a subordinate to diet, was for the treatment of
different lipid issue including primary hypercholesterolemia, mixed dyslipidemia, and segregated
hypertriglyceridemia [Jones et al.,2003].

1.5 Chemistry

Chemistry of rosuvastatin (rosuvastatin calcium) is a synthetic compound that comprises of a

solitary enantiomer which is constructed and administered as the calcium salt of the active
hydroxy acid, its chemical name is bis {(E)-7-[4-(4-fluorophenyl)-6-isopropyl-2-[methyl
(methylsulfonyl) amino] pyrimidine-5 yl] (3R, 5S)-3, 5-dihydroxyhept-6-enoic acid} calcium
salt. Identically, the exact equation for rosuvastatin calcium is (C22H27FN3O6S) 2Ca and
its atomic weight is 1001.14. The structural formula appears in Fig. 11. Furthermore,
rosuvastatin calcium is a nebulous white powder that is sparingly soluble in water and methanol
and marginally soluble in ethanol [Olsson et al.,2002].

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 Figure 1: Rosuvastatin Calcium [Gawad et al.,2013].

1.6 Pharmacology

In the same way, like other statins, rosuvastatin meddles with the synthesis of cholesterol in the
liver by obstructing the transformation of HMG-CoA to the cholesterol forerunner mevalonate.
This change is an early stage and the rate-restricting step is accelerated by the compound HMG-
CoA reductase. But, statins reversibly and aggressively restrain this progression through the
steric impediment of substrate attaching. Statin compound varies in their relative intensity for
hindering HMG-CoA reductase which relies upon, in addition to other things, the statins
fondness for the enzyme and the molecular fit of the statin to the compound restricted area. The
HMG-CoA-like side chain represents a significant part of the binding of the statin with the
enzyme. Similarly, by the means of polar cooperation, Synthetic statins and
rosuvastatin combine to the catalyst through their fluorinated phenyl group. Atorvastatin has an
extra restricting interaction with HMG-CoA reductase using a carbonyl oxygen particle, and
rosuvastatin has still additional restricting associations through its sulfone group. In many
studies, it has found that rosuvastatin has the best number and most exceptional kinds of limiting
collaborations with the enzyme’s active site which may clarify its more prominent hindrance of
the enzyme and its more prominent adequacy in bringing down LDL cholesterol than other
promoted statins. Around 85–95% of the HMG-CoA reductase hindrance related to rosuvastatin
is inferable from the parent compound [McKenney et al.,2005].

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Figure 2: Mechanism of action of Rosuvastatin [Abdeen et al.,2019].

1.7 Pharmacokinetics and Pharmacodynamics of Rosuvastatin

Rosuvastatin is only available in the tablet dosage form and administered orally. Still, in many
studies, there are no clinically meaningful differences that can be seen in pharmacokinetics
among the more aged and youthful or male and female patients, or between morning and evening
dosing. In vivo studies, it has been observed that the drug experiences negligible digestion. There
are no medically noteworthy interactions with known inhibitors of cytochrome P450 (CYP) 3A4
or other isoenzymes that are seen in medication collaboration.

It is suggested to administer rosuvastatin orally in the active form. After oral dosing, the parent
compound will reach peak plasma concentrations at 3 to 5 hours. On the other hand, in

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proportion to dose, both peak-plasma concentration (Cmax) and area under the plasma
concentration-time curve (AUC) are increased. The complete bioavailability of rosuvastatin is
around 20%. The mean volume of dissemination at a balanced state is about 134 L. On the
contrary, plasma protein binding of rosuvastatin is 88%, principally albumin; binding is
reversible and individualistic of plasma concentrations. The elimination half-life (t 1/2) is
roughly 19 hours. Usually, the pharmacokinetics and pharmacodynamics of rosuvastatin will not
seem to be overblown by the time of administration.

Rosuvastatin does not broadly metabolize; therefore, roughly 10% of an oral dose recuperated as
a metabolite. In studies with 14C-labeled rosuvastatin, 90% of an oral dose recovered
in faeces and 10% in urine. In faeces, 92% of the radioactivity was the parent compound, with N-
desmethyl and 5S-lactone metabolites representing 6 and 2% separately. The parent compound
represented roughly half of radiation, with N-desmethyl and 5S-lactone metabolites representing
20 and 10%, individually in the urine.  By and significant, 85–95% of dynamic plasma HMG-
CoA reductase prevent action which is denoted by the parent compound. In contrast to most
advertised statins, rosuvastatin displays insignificant association with CYP isoenzymes, and
experiences negligible hepatic digestion. Investigation of the impact of rosuvastatin 50 ìM on
CYP isoenzyme 1A2, 2C9, 2C19, 2D6, 2E1, and 3A4 movement in human hepatic microsomes
demonstrated no critical preventing impact on any [Olsson et al.,2002]. 

Table 01: Comparative pharmacokinetics of statins [Luvai et al.,2013].

Rosuvast Atorvast Simvast Pravast Fluvasta Pitavast Lovasta

Parameter
atin atin atin atin tin atin tin
Tmax (h) 3 2–3 1.3–2.4 0.9–1.6 0.4–2.1 0.6–0.8 2–4
Bioavailab
20 12 5 18 24 80 5
ility
Lipophilici
No Yes Yes No Yes Yes Yes
ty
Protein
88 80–90 94–98 43–55 >98 96 95
binding
Minimal Sulfation Minimal
Metabolis CYP3A
CYP2C9 CYP3A4 CYP3A4 Biliary CYP2C9 CYP2C8
m 4
CYP2C19 & urine CYP2C9

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 Biliary
excretion
excretion
Metabolite Active Active
Active Active Inactive Inactive Active
s (minor) (minor)

T1/2 (h) 19 15 2–3 1.3–2.8 1.2 10–11 2.9

Urinary
10 2 13 20 6 NA 10
excretion

Facial
90 70 58 71 90 90 83
excretion

1.8 Indication of Rosuvastatin

Rosuvastatin is considered as a standout amongst the most intense statins accessible for
decreasing flowing low-density lipoprotein cholesterol (LDL-C) levels. Its beneficial balance of
impacts on atherogenic and defensive lipoproteins and also its pleiotropic impact. In many
studies, it is found that rosuvastatin has anti-inflammatory and antioxidant effects. Progression in
endothelial dysfunction is related to decelerating of movement of atherosclerosis within the
artery wall and have been converted into clinical advantages for cardiovascular outcomes.
Rosuvastatin is having a beneficial impact on the progression of atherosclerosis over the clinical
dosage range of 2.5–40 mg. It diminished cardiovascular events in comparatively low-risk
subjects with raised high-affectability C-receptive protein and ordinary low-density lipoprotein
cholesterol. Similarly, as like other different statins, rosuvastatin is a proper treatment, besides
antihypertensive treatment, to lessen cardiovascular hazard in hypertensive patients [Hu &
Tomlinson, 2013].

1.9 Drug Interactions of Rosuvastatin

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As opposed to atorvastatin, lovastatin, and simvastatin, rosuvastatin experiences low to zero
digestion by the cytochrome P-450 (CYP) 3A4 isoenzyme system, However, it seems to have a
low probability for drug-drug collaborations with inhibitors or substrates of this enzyme.
Rosuvastatin endures small metabolism by the CYP 2C9 isoenzyme. Roughly 10% of a
radiolabeled dose is recuperated as a metabolite, for the most part, N-desmethyl rosuvastatin,
which has one 6th to one a large portion of the action of the parent compound. Simultaneous
administration of inhibitors of CYP 3A4 (e.g., ketoconazole, itraconazole, erythromycin) and
CYP 2C9 (e.g., fluconazole) has not exhibited noteworthy changes in the levels of rosuvastatin
found in the blood. Be that as it may, a few medications do antagonistically associate with
rosuvastatin, such as-

1.9.1 Cyclosporine

Heart transplant beneficiaries are treated with the immunosuppressant cyclosporine and get usual

doses of rosuvastatin 10 mg had a sevenfold increment in rosuvastatin mean AUC contrasted
with values obtained in healthy subjects. Therefore, patients taking cyclosporine are ought to get
close to 5 mg of rosuvastatin every day, and painstakingly observe for
potential unfavourable impacts. Equal treatment with cyclosporine and statins have been
appeared to expand the plasma concentration of different statins also, including atorvastatin and
simvastatin. 

1.9.2 Fibrates

The impact of gemfibrozil on the pharmacokinetics of rosuvastatin is like its impact on the
pharmacokinetics of the other advertised statins, except for fluvastatin. Healthy patients who
took gemfibrozil and a single dose of rosuvastatin exhibited 2.2-crease and 1.9 overlay increases
in rosuvastatin mean Cmax and mean AUC, separately. However, like different statins,
no remarkable changes in rosuvastatin AUC or Cmax were seen when rosuvastatin was co-
regulated with fenofibrate. Subsequently, fenofibrate should be considered as the fibrate of
choice when combination the treatment with a statin advisable.

1.9.3 Vitamin K antagonists

Co-administration of warfarin sodium (20 mg) and oral rosuvastatin (40 mg) as brought about an
expansion in the International Normalized Ratio (INR) of about twofold. There is one possible

9
clarification for this might be that since CYP 2C9 uses the two medications, a pharmacokinetic
collaboration results when the drugs give together. Especially for those patients who are taking
both warfarin and rosuvastatin, the INR ought to observe before rosuvastatin inception, after
dose modifications, and at interims generally prescribed for routine checking of anticoagulant
treatment. Even though any statin might influence warfarin's activities, rosuvastatin may have an
increasingly articulated impact on the INR.

1.9.4 Antacids

Co-administration of rosuvastatin (40 mg) with an antacid, there is decreased plasma

concentrations of rosuvastatin by over half; be that as it may, administration of the medications
two hours separated brought about no considerable change in plasma concentrations of
rosuvastatin [McKenney et al.,2005]. 

On the other hand, rosuvastatin combination treatment with fenofibrate, ezetimibe, omega-3-
unsaturated fats, antifungal azoles, rifampin (rifampicin), or clopidogrel is, by all means, safe, as
there is no proof to support any pharmacokinetic or pharmacodynamic collaboration of
rosuvastatin with any of these medications. Rosuvastatin, in this manner, has all the earmarks of
being moderately protected and very much endured.

1.10 Adverse effects of Rosuvastatin

Rosuvastatin shows high hydrophilicity and hepatic selectivity, just as low foundational
bioavailability while experiencing negligible digestion using the cytochrome P450 system. In
this way, rosuvastatin has an intriguing pharmacokinetic profile that is unique concerning that
different statins. Be that as it may, it stays to set up whether this may convert into a superior
wellbeing profile and fewer drug-drug interactions for this statin contrasted with others.
Likewise, with different statins, rosuvastatin treatment is related to generally low rates of
extreme myopathy, rhabdomyolysis, and renal failure. Rosuvastatin causes asymptomatic liver
enzyme elevations at a similarly low incidence to compare with other statins. Rosuvastatin
treatment has likewise related to unfavourable impacts identified with the gastrointestinal tract
and central nervous system, which regularly is seen with numerous different medications.
Proteinuria initiated by rosuvastatin is probably going to relate with a statin-incited hindrance of
low-molecular-weight protein reabsorption by the renal tubules. Maximum doses of
rosuvastatin are about cases of renal failure.

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Additionally, the co-administration of rosuvastatin with medications that expand rosuvastatin
blood levels might be harmful to the kidney. Moreover, rhabdomyolysis, considered a class
impact of statins, is known to include renal damage. But concerns have been raised by
discoveries from the JUPITER study proposing that rosuvastatin may somewhat increase the
prevalence of doctor-outlined diabetes mellitus as well as the levels of glycated haemoglobin in
elderly patients with various hazard factors and low-grade inflammation [Kostapanos et
al.,2010].

1.11 Laboratory and Clinical Efficacy

Rosuvastatin was observed to be exceedingly efficient in lowering plasma LDL cholesterol

levels and positively adjusting the other lipid and apolipoprotein parameters in patients with
hypercholesterolemia in both present moment and long-haul clinical trials. Also, in pairwise
correlations, rosuvastatin demonstrated altogether higher adequacy in diminishing LDL
cholesterol than milligram-equivalent doses of different statins right now accessible.

Dosing of rosuvastatin varying from 1 to 80 mg per day more than about a month and a half has
resulted in LDL-cholesterol reductions contrasted, and the benchmark esteems from 34% to
65%. But the LDL cholesterol reduction at the likely beginning dose range (5 to 10 mg) was 43%
to 51% [Olsson et al.,2001].

1.12 Clinical Trial of Rosuvastatin

In a straight similar trial, rosuvastatin or atorvastatin directed to patients with familial

heterozygous hypercholesterolemia. Where subjects were randomized to both 20 mg of
rosuvastatin or atorvastatin, and the portion was multiplied at 6-week time frames until all
patients achieved the highest dose of 80 mg for the two medications at weeks 12 to 18.
Reduction in LDL cholesterol fixations was essentially more notable for rosuvastatin contrasted
with atorvastatin at all time points, and 61% of patients taking rosuvastatin achieved target
objectives as indicated by NCEP-ATP II guidelines, compared with 46% of those taking
atorvastatin [Davidson,2002].

1.13 Quality Evaluation of Tablet

Tablet is a unit solid dosage form containing the active ingredient with or without suitable
excipient. These are the most widely used dosage form. The main objective of the design and

11
manufacture of the compressed tablet is to deliver the orally-correct amount of drug in the proper
form over proper time and at desired location, to have suitable chemical integrity protected at the
point of its action. The physical design, manufacturing process, and complete chemical makeup
of the tablet can have a profound effect on the efficiency of the drug being administered
[Sharma et al., 2017]. The evaluation of the physical characteristics of the pharmaceutical
products can ensure their quality as well as bioavailability and impart optimum therapeutic
activity. The maintenance of quality with continuous improvement in facilities is very important
in pharmaceutical industries because it is directly related to the healthcare system. Various
quality control tests are done to remove error from every stage, in production and maintain the
quality of the final product with the compendial standards as specified in the pharmacopoeias.
These include criteria for weight variation, disintegration, dissolution, content uniformity,
hardness, friability and uniformity of thickness [Kumar et al., 2016].

These tests categorized as following:

A. Official (Pharmacopeial) Tests:

 Uniformity of Weight

 Uniformity of Drug Content

 Disintegration Test

 Dissolution Rate [ Kumar et al., 2016].

B. Non-Official (Non-pharmacopeial) Tests:

 Hardness (Crushing Strength)

 Friability

 Uniformity of Thickness

 General appearance [ Kumar et al., 2016]. 

The weight of a tablet is determined by the quantity of fill in the die of a tablet press. The
variation of the weight of an individual tablet is a valid indication of the corresponding variation
in the drug content. The objective of the weight variation test is to ensure - good manufacturing

12
practices (GMP), appropriate size of the tablets and the content uniformity of the formulation
(Shabana, 2016).

Tablet requires a certain amount of strength or hardness and resistance to friability to withstand
mechanical shakes of handling in manufacture, packaging and shipping. Hardness generally
measures the tablet crushing strength. Hardness determinations are made throughout the tablet
runs to determine the need for pressure adjustments on the tabletting machine. Hardness can
affect the disintegration. So, if the tablet is too hard, it may not disintegrate in the required period
of time. And if the tablet is too soft, it will not withstand the handling during subsequent
processing such as coating or packaging [Badri and Gazi, 2016].

Tablet hardness is not an absolute indicator of strength since some formulations when
compressed into very hard tablets may produce chipping, capping and lamination problems.
Therefore, another measure of tablet strength i.e. friability is often measured, i.e. the friability A
friability test is performed to determine the ability of tablets to withstand abrasion during
packaging, handling, and shipping processes. A maximum weight loss, not more than 1%, is
generally considered as acceptable [Raka et al., 2016].

Disintegration is the first physical change observed for a drug when it enters into the body, thus
to see simulate the disintegration of the tablet in the body the disintegration test is performed. It
is the time required for the tablet to break into particles, the disintegration test is a measure only
of the time required under a given set of conditions for a group of tablets to disintegrate into
particles. In the present disintegration test the particles are those that will pass through a 10-mesh
screen. Complete disintegration occurs when no residue of the tablet still presents on the screen
except the insoluble ingredients as the shell or the coat of the tablet [ Kumar et al., 2016].

The definition of dissolution is deceptively simple. It is defined as the rate of mass transfer from
a solid surface into the dissolution medium under standardized conditions of liquid/solid
interface, temperature and solvent composition. It is a dynamic property that changes with time
and describes the process by which a homogenous mixture of a solid or a liquid can be obtained
in a solvent [ Kumar et al., 2016]. The study of dissolution used to assure the quality of solid
pharmaceutical forms for oral use, guarantee the quality from lot to lot, orientate the
development of new formulations, and secure the uniformity quality and performance of the
drug. This study allows formulation optimization in the development phase and it allows stability

13
studies, manufacturing process monitoring, and the establishment of in vivo/ in vitro
correlations. The evaluation of the dissolution profile could be auxiliary to the identification of
formulations that presented potential risk in relation to the drug bioavailability [Saptirini and
Rusniyanti, 2012]. The disintegration and dissolution process are illustrated in Figure 3.

Figure 3: The disintegration and dissolution process [Lerner et al.,2013].

1.13 Routine for Formulation Development and Stability Study

Goal of formulation development is to convert active drug moiety into suitable dosage forms.
This can be achieved by investigating of physicochemical properties of a drug substance alone
and along with excipients before the formulation. During development of stable and effective
dosage form it is not only depending on quality of API but also the careful selection of excipients
and selection of a good quality of excipient is also vital role in designing of good quality of
dosage forms. During this stage, selection of excipients is based upon their compatibility with
drug substance. Knowledge of drug excipient interactions is therefore very useful to the
formulator in selecting appropriate excipients [Honmane et al, 2017]. The product quality
changes with change in time due to certain environmental factors such as humidity, temperature
and light. The key objective of stability testing is investigation of those changes applicable to all
future batches of the drug product tested. It also helps to establish a shelf life for the drug
product. An ideal stability study should include the tests of all those attributes which are
susceptible to change during storage condition. The development and preparation of dosage form
is critical for patient safety and drug effectiveness. The stability of compounds may influence by

14
physical and chemical parameters such as presence of additives, storage conditions, and the
environmental factors such as temperature, humidity and light, these factors obtained major
concern in the manufacturing of drugs. Stability testing is an essential part of any drug
development. The purpose of stability testing is to investigate changes; stability plays an
essential role in the development of drug compounds [Khan et al., 2015].

1.14 Aim and Objective of the Study

The aim and objective of this study is to establish a comparative study between different
available brands of Rosuvastatin calcium 5mg tablet. This study would also be able establish a
conclusion that whether the different brands of tablet meets the official specification mentioned
in pharmacopeia. The current study was also designed to develop an immediate release
formulation of Rosuvastatin calcium 5mg tablet along with stability study. This study is
important to ensure that the drug provides better bioavailability, better drug release and better
stability for desired therapeutic effect.

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