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Basics of hypertension and available treatment. Overview of mechanism of action, risks/benefits of various classes of drugs. Prevalent prescription trends and future market review.
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CURRENT TRENDS IN HYPERTENSION THERAPY
Presented ByPOOJA SHARMA (M. Pharm Pharmacology)
Disease overview
• Hypertension (HTN) or high blood pressure, sometimes called arterial hypertension, is a chronic medical condition in which the blood pressure in the arteries is elevated.
• This requires the heart to work harder than normal to circulate blood through the blood vessels.
The Truth is
It is only a marker of the bigger problem
Hypertension is a multi-organ systemic disease
What we record as B.P.
The Problem is
Hypertension is asymptomatic in 85% of cases
What three factors contribute
to blood pressure?
Epidemiology
Hypertension: the world’s number 1 CV risk factor
• 7.6 million premature deaths worldwide
• 13.5% of global total deaths
• Causes more deaths than any other risk factor, including smoking or high cholesterol
Hypertension is the most powerful risk factor for cardiovascular morbidity and mortality
Global burden of disease
16 million
7–8 million
4–3 million
2–3 million
Global mortality
128 million
59 million
39 million
30 million
All cardiovascular
High BP
High cholesterol
Overweight and obesity
Ezzati et al. PloS Med 2005;2:e133
Hypertension is a leading cause of death and disability in all regions
Region Death Disability*
East Asia & Pacific 13.6% 6.5%
Europe & Central Asia 35.0% 19.6%
Latin America & The Caribbean 13.0% 5.1%
Middle East & North Africa 16.5% 6.1%
South Asia 9.6% 4.3%
Sub-Saharan Africa 4.0% 1.7%
Low-/ middle-income economies 12.9% 5.6%
High-income economies 17.6% 9.3%
World 13.5% 6.0%
Lawes et al. Lancet 2008;371:1513–8
BP is often not controlled, even when treated
0
10
20
30
40
50
60
70
80
Aware Treated Controlled
USACanadaItalySwedenSpainEnglandGermany
Wolf-Maier et al. Hypertension 2004;43:10–17* Threshold of SBP/DBP 140/90 mm Hg
Each 20/10 mm Hg BP increase doubles the risk of CV mortality
1-fold
2-fold
4-fold
8-fold
0
2
4
6
8
10
SBP/DBP, mm Hg
* Individuals aged 40–69 years (N = 1 million).Lewington S, et al. Lancet. 2002;360:1903–1913.
Hypertension adds to other CV risk factors
Other risk factors
SBP 120–129DBP 80–84
SBP 130–139DBP 85–89
SBP 140–159DBP 90–99
SBP 160–179DBP 100–109
SBP ≥180DBP ≥110
NoneAverage
riskAverage
riskLow
added riskModerate added risk
High added risk
1−2Low
added riskLow added
riskModerate added risk
Moderate added risk
Very high added risk
≥3, OD, MS or diabetes
Moderate added risk
High added risk
High added risk
High added risk
Very high added risk
CV or renal disease
Very high added risk
Very high added risk
Very high added risk
Very high added risk
Very high added risk
MS, metabolic syndrome; OD, subclinical organ damage
ESH–ESC Guidelines. J Hypertens 2007;25:1105–1187
Treatment goals and algorithms
Treatment Goal
The Truth is
Keep B.P. < 140/90 mm Hg in each patient
This may be revised to 120/80 may be ? 110/70
It is essential to keep the B.P at or below the goal
But, It also matters how the goal B.P. is achieved !
Goal BP
Current BP targets according to guidelines
JNC VII 2003 ESH-ESC 2007 WHO-ISH BHS IV 2006
<140/90* <140/90 SBP <140 <140/90
<130/80 <130/80 <130/80 According to national
guidelines
DM renal
DMrenal
post strokepost MI
DMrenalCVD
DMrenal CVD
* Lower if tolerated
Blood Pressure Classification
Seventh Joint USA National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure -JNC 7, JAMA, May 21, 2003, and USA Government Printing Office publication.
Hypertension treatment algorithm (JNC 7)
Hypertension treatment algorithm (ESH 2007)
Choose between
Low-dose 2-drug combinationLow-dose single agentNot at BP goal
Full dose ofsingle agent
Switch todifferent agent
at low dose
Full dose of2-drug
combination
Add athird drug
at low dose
Not at BP goal2–3 drugcombinationat full dose
Full doses of 2–3-drugcombination
Full-dosesingle agent
Marked BP elevationHigh/very high CV risk
Lower BP target
Mild BP elevationLow/moderate CV risk
Conventional BP target
ESH–ESC Guidelines. J Hypertens 2007;25:1105–1187
Approaching Hypertension
Pharmacologic treatment
Diuretics
Beta blockers
CCBs
ARBs
ACE – inhibitors
Enalapril
Lisinopril
Ramipril
Quinapril
Perindopril
Hypertension
Centrally acting agents
The Many Faces of HT Therapy Today
• Guidelines on the choice of agents and how best to step up treatment for various subgroups have changed over time and differ between countries.
• The best first line agent is disputed. The Cochrane collaboration, WHO and the US guidelines supports low dose thiazide-based diuretic as first line treatment.
• The UK guidelines emphasize calcium channel blockers in preference for people over the age of 55 years or if of African or Caribbean family origin, with angiotensin converting enzyme inhibitors used first line for younger people. In Japan starting with any one of six classes of medications including: CCB, ACEI/ARB, thiazide diuretics, beta-blockers, and alpha-blockers is deemed reasonable while in Canada all of these but alpha-blockers are recommended as options.
AGE
Younger (< 55)High Renin HT
Renin
ACEi, Beta-blocker Ca++-blocker, Diuretic)(AB/CD=
Dickerson et al. Lancet 353:2008-11;1999
Older (> 55)Low Renin HT
ACEi BB
A + B A + B + D
DiureticCCB
D + C + A D + C
I
II
III III
II
I
AB/CD Rule – HT Treatment
Each of the main classes of anti-hypertensive drugs affects the renin-angiotensin system
Brown. Heart 2007;93:1026–33
DiureticCalcium
channel
blocker
ACE inhibitor
Angiotensin receptorblocker
Beta-blockers
Kidney
ACE
Angiotensin I
Angiotensin II
AT1 receptor
Arteries – vascular tone
Na+
Renin
Angiotensinogen
++
ReninVolume
–
–
–
–
Bradykinin/NO
Inactive fragments
Angiotensin I
Angiotensin II
ACEI and ARBs block the renin-angiotensin system (RAS) in different ways
ARB
ACE-independentANG II formation by Chymase, etc.
AT2 RECEPTORVasodilationNatriuresis
Tissue regenerationInhibition of inappropriate cell growth
DifferentiationAnti-inflammation
Apoptosis
ACE ACE Inhibitor
AT1 RECEPTOR
VasoconstrictionSodium retention
SNS activationInflammation
Growth-promoting effectsAldosteroneApoptosis
SNS = sympathetic nervous systemHanon S, et al. J Renin Angiotensin Aldosterone Syst 2000;1:147–150; Chen R, et al. Hypertension 2003;42:542–547; Hurairah H, et al. Int J Clin Pract 2004;58:173–183;Steckelings UM, et al. Peptides 2005;26:1401–1409
DIURETICSFirst and Best Choice
Can be combined with A, B, C
βBlockersGood third Choice
Can be combined with A, D
Ca channel BlockersFourth Choice, Useful
Can be combined with D, A
ACEI and ARBSecond Best Choice
Can be combined with D, B, C
D
Diuretics
A
ACEI, ARB
B
β-Blockers
C
Ca-Blockers
D A
B C
The A B C D classes
KNOW ME WELL
I am ‘D’ for DIURETIC My Good aspects
Fluid depletion, Na washout, Low costImprove CHF, Systolic function, Ca savingReduce LVH, Morbidity & Mortality
My Bad aspectsPotassium washout, ↑ in Uric acid, ↑ CaAdverse on Lipids, Glucose control
Don’t use me inGout, HypokalaemiaDyslipedemia, Uncontrolled DM
DIURETIC
Diuretics help the kidneys eliminate excess salt and water from the body's tissues and blood.Loop diuretics:
Bumetanide, ethacrynic acid, furosemide, torsemide.
Thiazide diuretics:Epitizide, hydrochlorothiazide, chlorothiazide, bendroflumethiazide
Thiazide-like diuretics:Indapamide, chlorthalidone, metolazone.
Potassium-sparing diuretics:Amiloride, triamterene, spironolactone
Only the thiazide and thiazide-like diuretics have good evidence of beneficial effects on important endpoints of hypertension, and hence, should usually be the first choice when selecting a diuretic to treat hypertension. The reason why thiazide-type diuretics are better than the others is (at least in part) thought to be because of their vasodilating properties.
KNOW ME WELL
I am ‘A’ for ACEI and ARB My Good aspects
Improve Diastolic function, Systolic functionControl Proteinuria, Very favourable in DMImprove Coronary Ischemia, Good on
Lipids Reduce LVH, Morbidity & Mortality
My Bad aspectsBradykinin accumulation, Angio-edema↑ Serum K , ↓ GFR
Don’t use me inPregnancy, Creatinine is > 3 mg%, ↑ K
5.0 meqBilateral Renal Artery Stenosis, Angio-
edema
ACE inhibitors can be divided into three groups based on their molecular structure:
Sulfhydryl-containing agentsCaptopril , the first ACE inhibitorZofenopril
Dicarboxylate-containing agentsThis is the largest group, including:EnalaprilRamiprilQuinaprilPerindoprilLisinoprilBenazeprilImidaprilZofenoprilTrandolapril
Phosphonate-containing agentsFosinopril is the only member of this group
Angiotensin II receptor antagonists
Pressor inhibition at trough level - this relates to the degree of blockade or inhibition of the blood pressure-raising effect of angiotensin II.
However, pressor inhibition is not a measure of blood pressure-lowering (BP) efficacy per se.
The rates as listed in the US FDA Package Inserts (PIs) for inhibition of this effect at the 24th hour for the ARBs are as follows: (all doses listed in PI are included)
Valsartan 80 mg 30%Telmisartan 80 mg 40%Losartan 100 mg 25–40%Irbesartan 150 mg 40%Irbesartan 300 mg 60%Azilsartan 32 mg 60%Olmesartan 20 mg 61%Olmesartan 40 mg 74%
I am ‘B’ for βBlocker
My Good aspects ↓Heart rate, ↓Force of contraction, ↓Conduction ↓Myocardial O2 demand, Improve Ischemia
Improve QUALY in CHD, Useful in CHF, Migraine My Bad aspects
Constrict peripheral vessels, BradycardiaUnfavourable on Lipids, Glucose
Don’t use me inBradycardia, Conduction defects, Caution in CHFPrinzmetal Angina, MSD, PVD, BA, COPD, Dys
lipidPheochromocytoma, Chronic smokers
β Blocker KNOW ME WELL
Nonselective agentsAlprenolol, Bucindolol, Carteolol, Carvedilol (has additional α-blocking activity)Labetalol (has additional α-blocking activity), Nadolol, Oxprenolol (has intrinsic sympathomimetic activity), Penbutolol (has intrinsic sympathomimetic activity)
β1-selective agentsAlso known as cardioselectiveBetaxolol, Bisoprolol, Celiprolol, Esmolol, Metoprolol, Nebivolol (also increases nitric oxide release for vasodilation)
β2-selective agentsButaxamine (weak α-adrenergic agonist activity): No common clinical applications, but used in experiments.ICI-118,551: Highly selective β2-adrenergic receptor antagonist—no known clinical applications, but used in experiments due to its strong receptor specificity.
β3-selective agentsSR 59230A (has additional α-blocking activity): Used in experiments.
KNOW ME WELL
I am ‘C’ for Ca channel Blocker
My Good aspectsVasodilatory, Suitable in elderly, Low costAnti arrhythmic (Verapamil), ↑Coronary BF (Diltz)Neutral on lipidemia, Vasospastic Angina
My Bad aspectsFluid retention, Impair failing heartAdverse on Glucose control.
Don’t use me inTachycardia, arrhythmias, CHF, Uncontrolled DM, Volume overload
• Dihydropyridine CCBs are often used to reduce systemic vascular resistance and arterial pressure, but are not used to treat angina because the vasodilation and hypotension can lead to reflex tachycardia.
Amlodipine, Aranidipine, Azelnidipine, Barnidipine, Benidipine, Cilnidipine, Clevidipine, Isradipine, Efonidipine, Felodipine, Lacidipine, Lercanidipine, Manidipine, Nicardipine, Manidipine, Nicardipine,Nifedipine, Nilvadipine, Nimodipine, Nisoldipine, Nitrendipine.
• Phenylalkylamine CCBs are relatively selective for myocardium, reduce myocardial oxygen demand and reverse coronary vasospasm, and are often used to treat angina.
Verapamil • Benzothiazepine CCBs by having both cardiac depressant and
vasodilator actions, are able to reduce arterial pressure without producing the same degree of reflex cardiac stimulation.
Diltiazem (Cardizem)• Nonselective mibefradil, bepridil, fluspirilene, and fendiline.
RENIN INHIBITORS• These drugs inhibit the first and rate-limiting step of the renin-
angiotensinaldosterone system (RAAS), namely the conversion of angiotensinogen to angiotensin I.
• Aliskiren is effective in lowering blood pressure, but as of 20 April 2012 the US Food and Drug Administration (FDA) issued a warning of possible risks when using aliskiren or blood pressure medicines containing aliskiren with ACE inhibitors and angiotensin receptor blockers (ARBs) in patients with diabetes or kidney (renal) impairment. They advised that such drug combinations should not be used in patients with diabetes because of the risk of causing renal impairment, hypotension, and hyperkalemia and that aliskiren should not be used with ARBs or ACE inhibitors in patients with moderate to severe renal impairment. However, they also recommend that patients should not stop taking aliskiren without talking to a healthcare professional.
• Aliskiren in combination with hydrochlorothiazide was approved by the FDA in 2008
The importance of treatment adherence
Patients who are adherent are more likely to attain BP control
Controlled BP (%)
* <140/90 mmHg or <130/85 mmHg for patients with diabetes
Bramley et al. J Manag Care Pharm 2006;12:239–45
0
5
10
15
20
25
30
35
40
45
50
Low (<50%) Medium (50-79%) High (>=80%)
45% greater probability of control
Adherence(n = 165)(n = 46) (n = 629)
Treatment adherence is highest with ARBs
ARB, angiotensin II receptor blocker; CI, confidence interval* Relative to ACE inhibitors after 1 year of treatment
Corrrao et al. J Hypertens 2008;26:819-24.
0.5 1.0 2.0
Diuretics
β-blockers
α-blockers
Calcium channel blockers
ACE inhibitors
ARBs
1.83
1.64
1.23
1.08
1.00
0.92
- +Cause-specific hazard ratio (95% CI) for discontinuation*
Total n = 445,356
Persistence with hypertensive therapy
Monotherapy or combination treatment for hypertension
• Antihypertensive monotherapy is effective in only
about 40-60% of hypertensive patients, irrespective of
the category of the agent that is used.
• Most of the responders are Stage I hypertensives.
Therefore, there is frequently a need for the use of
two medications with different mechanisms of action.
• Should therapy be started with two drugs or a
combination?
Monotherapy
Average no. of antihypertensive medications
1 2 3 4
Trial (SBP achieved)
ASCOT-BPLA (136.9 mmHg)
ALLHAT (138 mmHg)
IDNT (138 mmHg)
RENAAL (141 mmHg)
UKPDS (144 mmHg)
ABCD (132 mmHg)
MDRD (132 mmHg)
HOT (138 mmHg)
AASK (128 mmHg)
The majority of hypertensive patients need combination therapy to achieve their BP target (SBP)
Bakris et al. Am J Med 2004;116(5A):30S–8 Dahlöf et al. Lancet 2005;366:895–906
Hypertension – Why Combinations ? If goal BP is not achieved by a single drug in full
dose
Then adding another agent will help achieve the goal BP
Two agents sometimes nullify each others side effects
Fixed dose combinations will reduce the no. of tablets
Once daily formulations are good for compliance
Sustained release or Long Acting formulations for 24 h BP control
If three drugs can’t achieve goal BP – Resistant HT
Diuretics
β-blockers
α-blockers
ACEi
CCB
ARB
Adapted from Mancia et al. J Hypertens 2007;25:1105–87Manchia et al J Hypertens 2009; 27: 2121-58
Diuretics
ACEi
CCB
ARBONTARGETACCOMPLISHHYVET
2007
2009
ESH-ESC treatment recommendations
Drug Combinations
Hypertension – Rational Drug Combinations
ACEI and ARB = A
Beta Blockers = B
Calcium Channel (CCB) = C
Diuretics Drugs= D
D and A combination is excellent - Ramace H, Losar H, Enace D
D and B combination second - Betaloc H, Atecard D, Tenoric
D and C combination sixth - Amlogaurd H, Stamlo D
A and B combination Third - Losar A, Cardif Beta
A and C combination fourth - Amlopres L, Hipril A, Amlo LS
B and C combination fifth - Amlo AT, Amlobet, Beta Nicardia
Diuretics = D – Rank 1
ACEI and ARB = A – Rank 2
Beta Blockers = B – Rank 3
CCB = C – Rank 4
Some Irrational Combinations
Beta blockers + Beta1 stimulants - Rebound HT, Paradoxical BP ↑
Beta blockers + Vepapamil - Extreme bradycardia, HB, CHF
Thiazide + Furesemide - Potential volume ↓ and K ↓
CCB + Thiazide- No RCTs to support the additive
Prazocin + Beta blocker - They nullify the effects of each other
Verapamil / Dilzem + Nefidepine -No rationale (cardiac actions contridic)
Beta blocker + ACEI Not for HT alone, Good for CHF, MI, IHD
Sub clinical doses of two drugs Try one drug in good dosage, then add
Two drugs of same class - No rationale (like Enalapril + Ramipril)
(Atenelol + Metoprolol, Nefidepine + Amlo)
Incidence of New Onset Diabetes with Various Medications.
How significant is it?
Risk of Hyperglycemia with Use ofAntihypertensive Drugs
Thiazide
Central antiadrenergic agents
Peripheral antiadrenergic agents
ACE inhibitors
B-Blockers
Calcium channel blockers
Vasodilators
>1 Agent without thiazide
>1 Agent with thiazide0.5 1 1.5 2 2.5 3
DecreasedRisk
IncreasedRisk
Adjusted ORs and 95% CIGurwitz J H. Arch Intern Med 1993;118:273-278
DecreasedRisk
IncreasedRisk
Ongoing trends
Review of companies and drug classes in the 2007–2011 antihypertensive patent literature
Future treatment options
Orally Active Aminopeptidase A Inhibitor -- a
Prototype for a New Antihypertensive Drug Class
• RB150, an orally active prodrug that inhibits brain but not
systemic renin-angiotensin system (RAS) activity, reducing
blood pressure in an experimental animal model, is reported.
• Previous research indicated that in the brain, conversion of
Ang II to Ang III, which is catalyzed by aminopeptidase A
(APA), is a necessary step in increasing blood pressure. They
used specific and selective APA inhibitors to show that Ang III
is one of the main effector peptides of the brain RAS ,
exerting tonic stimulatory control over BP in hypertensive
rats. APA, therefore, is a potential therapeutic target for the
treatment of hypertension.
Identification of Angiotensin-Converting Enzyme-2
Activators as Potential Antihypertensive Drugs
• ACE 2, a homolog of ACE, is a key RAS enzyme involved in
balancing the adverse effects of angiotensin II on the
cardiovascular system. It is known to degrade angiotensin II
(Ang II) to generate angiotension which has vasodilatory and
antiproliferative effects. Blocking AngII with ACE inhibitors or
angiotensin receptor blockers (ARBs) has been shown to
increase cardiac ACE 2 expression.
• Altered expression of ACE 2 is associated with cardiac, renal,
and vascular dysfunction.
Slow-Releasing Hydrogen Sulfide Compound With Potential as Antihypertensive Therapy
• Hydrogen sulfide (H2S) is known to have cardiovascular effects such as the ability to dilate human blood vessels and protect the heart against ischemia/perfusion injury, and it also plays a role in hypertension.
• Researchers have identified a slow-releasing H2S compound that mimics the generation of H2S in vivo.
• In addition, the blood pressure lowering effect of the compound is without affecting heart rate and withoutweight loss or other signs of toxicity, suggests that it, or a compound like it, may be of a therapeutic benefit in cardiovascular disease.
• The compound GYY4137 was found to release H2S slowly both in aqueous solution in vitro and after intravenous or intraperitoneal administration in anesthetized rats in vivo.
• It caused a slow relaxation of precontracted rat aortic rings and dilated the perfused rat renal vasculature by opening vascular smooth muscle adenosine triphosphate-sensitive potassium (KATP) channels.
• Aliskiren is a novel, completely nonpeptide, orally active renin inhibitor that blocks the first and rate-limiting step of the renin-angiotensin system.
• Alagebrium, an advanced glycation end product (AGE) crosslink breaker, has been shown to reduce SBP in patients with uncontrolled systolic hypertension.
• Progestin drospirenone and 17 beta-estradiol (DRSP/E2), developed for postmenopausal hormone replacement therapy, has been shown to lower both clinic and ambulatory SBP in postmenopausal women .
Antihypertensives Market to 2016 - Generic Erosion Following Patent Expiry of Major ARBs to Impact the Market
The global market:
overview, opportunities and threats
The Global Anti-Hypertensive Market is Set to Show Flat Growth in the near Future
In 2009, the global anti-hypertensive market was estimated to be worth $27.2 billion, representing a Compound Annual Growth Rate (CAGR) of 5.0% between 2002 and 2009. The market is forecast to reach $30 billion by 2016, indicating a CAGR of 1.5% between 2009 and 2016. The primary reason for slight and gradual growth in the market is the patent expiries of major blockbusters, which are expected to decrease the annual cost of therapy after 2007.
The global anti-hypertensive market is expected to witness a series of patent expiries between 2007 and 2015, which includes most of the top selling blockbuster drugs in the anti-hypertensive market. The major drugs that are set to lose patent protection include Novartis’s Diovan (2012), Sanofi Aventis’s Avapro (2012), Novartis’s Exforge (2012), Takeda/AstraZeneca’s Blopress/Atacand (2012), Pfizer’s Revatio (2012), Actelion’s Tracleer (2015), and United Therapeutics Remodulin (2014).
All these drugs together accounted for more than $19.4 billion in revenues in 2009. Merck’s Cozaar patent expired in April 2010. The sales of Cozaar for the year 2009 were $3.6 billion. Pfizer’s Norvasc, which was once the world’s most prescribed drug for hypertension and angina, saw a sales decline of 12% in 2009 due to genericization in 2007. Thus, the series of upcoming patent expiries in the hypertension as well as PAH markets are set to lead to a decline in the market in the near future. However, due to increased usage of fixed dose-combinations and the entry of generics, the market is expected to rise slightly after 2015.
The current anti-hypertensive pipeline does offer some promising novel products, such as SPP635, Actos, LCZ696, QT1571, ACT-293987, PS-433540, Macitentan and Riociguat, indicated for the treatment of hypertension and PAH. However, the revenues generated from these products are not expected to completely make up for the revenue losses due to patent expiries. Thus, the overall global anti-hypertensive market is expected to show flat growth during the forecast period.
Top Six Companies Control Approximately 74% of the Market
The current global anti-hypertensive market is significantly consolidated as the top six players control approximately 74% of the market. Novartis is the current market leader with its blockbuster product, Diovan. It is available in more than 100 countries. It has recorded sales of six billion in 2009. Other major products in the anti-hypertensive market of Novartis are Exforge, Tekturna/Rasilez, Lotrel and Lescol, controlling 43% of the total anti-hypertensive market. Merck follows Novartis with a 19% market share, primarily due to its top selling ARB, Cozaar. The sales of Cozaar are set to decline in the future as the patent on Cozaar expired in April 2010. Pfizer occupies the third position with its blockbuster drug Norvasc. Pfizer also marks its presence in the PAH market with its Revatio. Norvasc went off-patent in the year 2007. It was one of the blockbuster drugs in the anti-hypertensive market until this date. Takeda is the fourth player in the anti-hypertensive market, with its blockbuster drug Blopress.
The sales of Blopress are set to increase in the coming years. Takeda is followed by Actelion and Sanofi Aventis. Actelion is the market leader in PAH with its blockbuster drugs, Tracleer and Ventavis. Actelion and Sanofi Aventis control 8% and 7% of the total market. However, the market shares of the total players are expected to witness changes in the near future due to upcoming patent expiries. Novartis’s Diovan and Tekturna/Rasilez are set to expire in 2012. Exforge is set to expire in 2010. Merck’s Cozaar went off-patent in the year 2010. Merck and Pfizer have been registering negative growth in recent years due to patent expiries. Novartis, Takeda and Actelion have shown positive growth.
• The growth rate of the antihypertensive market is declining. These changes reflect the challenges faced by pharmaceutical companies over the next decade, as brand erosion and healthcare reforms impact heavily.
• The slow and declining growth rate does not reflect a stationary market, but the battle between the drugs that make up the market.
We are still evolving towards finding an Ideal Antihypertensive