Thursday saw the delivery of a new Novartis drug: Tekturna (aliskiren). None of us had any idea what it was for, so we looked it up on Facts and Comparisons, and there was next to no information whatsoever, except that it is a “direct renin inhibitor” — whatever that meant.
Now that I’m home on a non-firewalled Internet connection, I can actually get real drug information. (How sad is it that I can’t do this at the pharmacy?) Aliskiren:
Aliskiren is a direct renin inhibitor, decreasing plasma renin activity (PRA) and inhibiting the conversion of angiotensinogen to Ang I. Whether aliskiren affects other RAAS components, e.g., ACE or non-ACE pathways, is not known
I’m sure you could play games targeting specific points and pathways in the renin-angiotensin-aldosterone system until the cows come home, but how many of them will be meaningful? Medscape has an article comparing, contrasting, and using Diovan and Tekturna in parallel:
Do we need Tekturna? Would not an ARB plus a diuretic do a better job? There are benefits to combining an ACEi with an ARB, that are fairly well understood. Is Tekturna going to create some sort of super trifecta?
I’m thinking not. Combining an ACEi with an ARB does a couple of things. First off, ACE inhibitors only stop the conversion of angiotensin I to angiotensin II. Blocking the pathway there does nothing to stop any non-specific binding to the angiotensin II receptor sites. ARBs block much of this non-specific binding because the receptor sites themselves are blocked. However ACEis also block the breakdown of bradkinin (which is broken down by ACE) which leads to greater vasodilation, which is why ACEis and ARBs are usually similar is study results. Bradykinins, of course, are a double-edged sword: they may contribute to vasodilation, but they are also responsible for the dry cough and angioedema associated with ACEis.
I don’t see how aliskiren is going to add to this. Is there component to the RAAS that I’m not thinking of? Is it not better to attack a problem from many different angles instead of hitting the same pathway three different ways?
“Is it not better to attack a problem from many different angles instead of hitting the same pathway three different ways?”
Of course it is, but that would require more basic science, ie, actual research; which costs money. The only thing better than a “me-too” drug is another drug that hits the same pathway somewhere else. See? It’s different (even though its end result is the same.) The pharma R&D “path of least resistance” is the path of least expense.
Using and ARB and a diuretic to achieve the same thing is NOT just as good. We know diuretics ACTIVATE the RAAS and that is why we try to avoid giving them. Not to mention that they increase blood glucose, decrease GFR and cause electrolyte abnormalities. So maybe Aliskeren would be better….only time will tell.
Julie,
Diuretics may activate the RAAS, but this is largely mitigated by the use of an ACEi or an ARB. It becomes an excercise in pointlessness to nail the same pathway three different ways (in most cases). Once or twice is enough. After that, you’re better off exploring other ways of lowering blood pressure. (CCBs, diuretics, beta blockers, etc.)
This is especially true in patients whose HTN isn’t mediated by the RAAS. But you knew that already.
I love Tekturna. A 150 mg dose lowered by SBP from the 160s to the 120s with no noticeable side effects. I cannot take either ACE inhibitors or ARBs because both give me unbearable muscle pain. (The ACE inhibitors are worse than the ARBs.) I am also allergic to sulfa drugs so cannot take diuretics.
I’ve been taking Lotrel for quite some time and the results have been just ok. I started on a 300 mg dose of Tekturna plus
160 mg of Diovan 6 days ago in place of the Lotel, and my numbers have shot up significantly. I’ve been told to give it 2 weeks. I’m not encouraged at this point. It seems over time that
the only family of medicine that has an impact is the CCB’s.
It could be that your HTN is not mediated by the RAAS, which is quite common among African Americans, for example. The lack of efficacy of drugs which target the RAAS would seem to indicate that this is the case. *shrug*
There are millions of people who have hypertension and remain uncontrolled. Tekturna is a new option. Why not stop the RAAS at the point of activation. Tekturna can also reduce plasma renin activity by 50-80% and hypertensive patients have higher renin plasma activity. Granted there are alot of options for reducing blood pressure but reducing PRA down to a normotensive patient level that you have to admit is exciting news. I’m all for having Tekturna used first line or add on for the additional benefit of lowering blood pressure and PRA.
all of the different classes of HTN med’s (at comparable dosing strengths) show similar BP reductions. You failed to mention the fact that Aliskiren has a very favorable side effect profile. The fact that you have the ability to add on to any other Anti-Hyptertension med, and not have an increase in side effect, makes this a very attractive add-on therapy for those not controlled.
Recent studies suggest that the average Hyptertension patient needs an average of 3 different classes to acieve BP controll. A new class that has “equal” BP reductions in monotherapy, added reductions on top of ANY other agent, and a very favorable side effect profile should make this an attractive drug right away.
You might also want to look at this drug’s long lasting effect. Given its 40 hr. half life, this is a true once a day medication, with consistent 24 hour control, without any rebound hpertension after 2 days following discontinuation.
(another very favorable trait about Aliskiren)
What I’m reading and hearing about the expected end-organ bennefit from this class gives even more hope for the future.
Overall, I’d say that the future looks bright with this new addition to the HTN marketplace, so I disagree with your original assessment.
Just had to say that I find it funny that a “Pharm D” would not see the benefits of attacking a problem at the rate inhibiting step. That is exactly what aliskiren does. As far as I am concerned, all new weapons for treating HP are beneficial and needed. Really looking forward to seeing how direct renin inhibition might change how we treat HBP!
Could someone tell me what the implications of the Pro-Renin Receptor may be? (HINT)
How would Tekturna come into play? (HINT)
This is a good drug, and a class that is a big part of the future of treating Hypertension. The future is bright for the DRI class of drugs.
Tekturna hasn’t done sqaut for me. It doesn’t lower my bp and doesn’t last 24 hrs.
Thats really funny!! Doesn’t last 24 hours!? I think you may be taking the placebo pill…
Tekturna does both very well, and doctor’s are jumping onto the DRI/Tekturna bandwagon very quickly!
i have been taking Tekturna for eight dats along w/ atacand 32/16 pressure is still the same, nothing seems to take my systolic down it stay high. I have been on all major BP medicine helps.
I believe they was giving me wrong medicine together. I need to know why no one can get my pressure under control? My legs hurt terrible. I am sleeping all of the time
Hyperkalemia…. i see that as a significant problem, and hypotension is increased with higher dose aces and atorvastatin. I don’t see how having a patient on an ACE, ARB, and this is going to increase efficacy, i believe we’ll be seeing a lot of people having renal problems if we con’t to bombard certain pathways that may not even be the cause of the problem to begin with. I agree, a “me too” drug.
My dr. has just put me on this & I seem to be very dizzy all the time.
What is the best time of day to take a blood pressure medicine; as he never said nor the pharmacist.
Thank you.
B. Marcom
Barb, some people find that if they become dizzy, it is best to take the medication at bedtime so you sleep through the side effects. If you are on a diuretic, make sure you do not become dehydrated, this can happen when people are placed on other BP medications. You should contact your provider to let them know you are having this symptom.
Because it doesn’t matter. But it doesn’t hurt to, you know, ASK next time.
I can’t believe that the introduction of this drug caught anyone by surprise. Its been hyped in all of the publications for months, since it is the first of a new drug class for HTN.
Just as we are finding some benefit to combining an ACE and an ARB (early on no one thought this needed to be done) I think there will be benefit in combining Aliskiren with an ACE or ARB for more complete blockade.
I have a tekturna question for the whole gang! I’m doing a market research project on drugs for dyslipidemia. Who is paying for your Tekturna? I’m trying to find out what managed care formularies it is already listed on. So is insurance paying for it? If so, who is your provider? Thanks in advance!
Kath
I have been on tekturna 300 mg for 3 months- an dit is the only medication that is working- I also have the clinidine patch which does well with tekturna. NOthing else had worked , I have no side effects and it lasts for the day. I am thankful for the medication- ARBS, BETa Blockers and ACE caused me numerous problems or didn’t work…
I have been on Tekturna for six weeks and have noticed that my BP is controlled nicely during the day but is elevated before bed and upon awakening. What could be causing this? Menopause? As far as side effects go, I have started to feel very achey and tired. I haven’t noticed anyone else writing with this complaint. I have a normal renin level and one kidney.
is there DR OR NURSE OUT THERE THAT CAN explain to me these terms and what they do? ARB, RAAS, PRA, ACE AND NONE ACE INHIBATOR, REINN INHIBATOR IT SAID DECRESS PLAMSA, RENIN ACTIVATE PRA INHIBITING THE CONVERDION OF ANGROTINSINOGEN ANG1. PLEASE EXPLAIN
I HAVE BEEN TAKING TEKTURNA FOR OVER A MONTH ALONG WITH WATER PILL AND DIVON MY PRESSURE SEEMS TO HAVE GONE DOWN 10 POINT BUT STILL HIGH.
I DID NOTICE THAT IT WORKS BETTER WITH THE PLINDEL BUT IT GIVES ME A HEADACHE AND MAKE ME SO TIRED
SOME ASK WHO PAYES FOR THIS MY INSURANCE CO.NGS
NAOMI
I have been on tekturna for 3 months. I wake with hives, and sometimes swelling of lips. This will last until i take allegra. anyone else with this problem?
That means you’re mildly allergic to the drug, and should take something else.
You are having angioedema which can be a lifethreatening reaction to this medication. You should stop Tekturna and contact your provider immediately and continue to take the allegra.
I just started taking Tekturna today. I went down to have my blood pressure taken here at work and my blood pressure went from 187/92 (two days ago) to 140/74 (today). This is quite a drop and will definately report back in about 2 weeks to let you know what it is then. I could feel the pill “kick-in” this morning (7:30am)today with some dizziness about an hour and 1/2 after taking one 300 mg. pill. But I feel very relaxed now with no dizziness (3:52pm).
I have no doubt the drug works. I just question its value in the light of the alternatives. See my other Tekturna post for details.
Just give this new class of antihypertensives time. From what I read in there may be some significant benefits in the future such as better renal function, less ace-induced cough (in combination with an ACE-I), and the half life of this medication is phenomenal considering that no other class of antihypertensives even comes close. I know I forget my bp medication all the time. On Tekturna I have CV protection for days when I miss a dose, and we know that with BP being asymptomatic, BP medication is easy to forget.
Have been on Tekturna about a month. My side effects increase:muscle weakness(have resorted to back brace for temp relief),fatigue,difficult to wake up,mental fog,ache from head to toe,but my top number is now in normal range. Anyone else feeling this way?
I did not see any sexual side effects mentioned in the literature; this is an important consideration, any data available?
Tekturna is wonderful for people who are allergic to RAAS pathway drugs (ACE inhibitors and ARBs)and who are also allergic to sulfa drugs (and therefore to diuretics). I take Tekturna along with Metoprolol (a beta blocker). I was not allergic to calcium channel blockers but they simply did not lower my systolic number. I am very grateful that Tekturna was discovered because I think my isolated systolic hypertension is due to an overactive RAAS pathway.
I am very hyper-sensitive to all meds but have high blood pressure. I feel everything……220/140’s and UP…I take clonidine in the ER when it’s this high…….I have been admited to the hospital twice for high BP..White male, 37 years old……Mom had two heart attacks and both arteries in neck were blocked, dad had triple bypass recently both before age 50..both are thin but smoked……I don’t do drugs, smoke,or drink…
I started this drug today (sept 10, 2007 ) and within a half an hr, I am dizzy, sweating really bad, and I have a metallic taste in my mouth, my lips feel a little sunburned, maybe sweeling…
I just stopped micartis hct and I was on Inderal, Norvasc, lotensin, HCT by itself, then Lotrel, then aetenol, Diovan,
the doctors find it easier to seperate the drugs……..all thse drugs cause me to have severe stomach pain and all of them but Inderal and Aetenol made my heart race.
What is funny is that I was on lotrel for years, no side effects…I lost 60lbs, I didn’t need it anymore, I found the weight again and started it over, severe headaches, ANXIETY and racing heartbeats…….for 3 weeks…doc is confused!……Gave me Inderal as needed, this caused me to feel like I was having a heart attack everytime I tried to move from a sitting to standing position.
then we seperated the lotrel and used lower doses…NOPE!, BUT>…….the high heart rate made me drop 20lbs quickly..I had to eat 0.05mg of Ativan 3 to 4 times daily to take the anxiety away….but…….before this I was on NO MEDS and weight went from 240 to 300lbs in a year with maijor lifestle chnges, no fast food, I walk daily, no soda, switched from whole milk to 2%, to 1% to skim…weight stayed the same…..no idea why…….trigs went down, chloesterol went down, all blood work is good but weight stays the same,….I barely eat and get full quick…..ultra sounds of belly, ct of belly, found kidney stones…they have passed which caused me to have a UTI for 3 months………..now my docs want to recheck my kidneys due to all this blood presure problem
if anybody has any ideas let me know…Victor….bbailey60@cfl.rr.com
6pm………….worst medicine ever, I guess it peak is about 3-4 hrs……..severe stomach cramps and then about an hr on the toilet….I barely made it..I have severe pressure in my jaw and my left side of my face is bright red…..blood presure is 134/84/143..pulse is high……..WHY?…….I took ipecap and then activated charcoal but it was too late,….I will never take this medicine again.. I will start my micardis tomorrow without the HCT….I can’t handle this…I felt better when I was ready for a stroke..
I am interested in hearing if other people have had a decreased sex drive with taking Aliskiren and Valsartan combination. Do taking blood pressure medication have an affect on sex drive?
Indeed, most BP medications have impotence listed as a side effect; I see it often in my patients, hence the question earlier about the side effect profile for tekturna. Any pharm folk comment?
RAAS drugs are the most ED-friendly anti-hypertensives out there, it seems. Especially compared to CCBs, for instance.
In general, restoring the RAAS to normal (rather than hyperactive) function improves endothelial function — a key component in impotence. This is true for both ACE inhibitors as well as ARBs, so it stands to reason that it’s a pathway effect, which means aliskiren should follow in the other class’ footsteps. This means that symptoms of erectile dysfunction *should* decrease as therapy continues, as opposed to getting worse. Of course, there are always the statistical outliers, and decrease libido does happen in a small minority of patients.
Unless there’re things (either good or bad) that we don’t know about Tekturna yet that will only come to light as prodigious data are made available over time. (Coxibs and their effect on polyp formation comes to mind.)
As with any drug, the first week is usually the worst in terms of side effects as you and your body adjust.
hi all
i was on this drug almost 4 weeks,the first time i took it my heart went into tachycardia within 5 hours.i went to ER told me nothing was wrong,doctor said rapid heart rate wasn’t a side effect.continued to take it for 25 more days almost went into cardiac arrest palpitations an tach were so bad when i went to ER they had to put me under.told me to discontinue and never take it again.it’s been 2 weeks and the palpitations and tach is still there but nothing near the way it was.have had the same effect with ccb’s but never this severe i thought my heart would explode i’m diabetic ,hbp, kidney disease (you know the combo meal)the doctor has no idea how long this crap stay’s in your system or the damage it may have caused.
I want to know about the long tem effect i.e localized production of angiotension II. Just like the ACE escape. If receptor cites are blocked, this alone would be the most potent agent against the effects of angiotension II. I am not against Tekturna- any more weapons are great, but lowering BP alone is the best defense & targeting another pathway CCB would trigger better reductions. Most need volume control so they will be on a diuretic and you know they will be one an ACE or ARb. The best info. we will see will be when ONTARGET comes out.
I am amazed at the lack of knowledge that is showing up on this site. Mr. RJS…..do your homework. As a pharmacist you were taught to look at the rate inhibiting step. DRI does just this. We have been looking for this for decades and now that it is here we should be blessed to live in a time that we can treat the RAAS in such a complete way. There are thousands out there that are having MI’s and massive coronaries each today. If DRI along with ARB’s would have been available to them 20 years ago they might be out of the hospital and palying with their grandchildren. PLEASE….PLEASE….do not discount this tool. Watch and see!!! As the massive amounts of data floods out I hope you are hear to eat your words!!!!
Did my homework. Still not impressed. I’m sure the drug works as advertised. There just isn’t a niche for it except for those rare folks who can’t take an ACEi or an ARB.
Tekturna offers no benefit over ACEi or ARB (or ACEi + ARB). I’m sure there will be an ocean of data that says it’s as good as the ACEis or the ARBs. I am skeptical that there will be any data that says Tekturna is better than its competition in head to head trials.
If you come across any, let me know. I’ll be waiting. (Probably for a long time.)
Dear Dr RAAS, Sorry you are so angry and are sucked into the amount of drug company b.s. that has brainwashed you! Tekturna is a new agent, fine. In studies it will never be compared *statistically* to any other inexpensive/generic drug. In the combination study with HCTZ, it was only better at lowering DBP. However, the placebo response was also very high, so considering the placebo effect only about 1/3 of patients could be considered as responders! The HCTZ group in this study lowered SBP and DBP as much as 150mg and 300mg of tekturna!
Lack of knowledge comes from not being able to critically evaluate the literature. Don’t be blinded by the infamous twist that drug companies do to push these agents, this is why we’re in the mess that we’re in today.
Oh, and the last time I checked a “massive Coronary” is the same as an MI. and if you want to “cut down” Mr. RJS, then learn how to spell HERE (place) HEAR (action).
Aliskiren as a “me to”. AS far as my typo….when you have been on call 24hrs you might tend to have a slip of the finger. Now..pertaining to the data to revealed in regards to DBP reductions in comparing DRI to HCT. First…do you understand the Renin system and its effect on BP. Probably not!! The thing is. We have been chasing numbers for decades and low and behold we have only managed to …say in the HOPE trail benefit about 20% of the patients. Do you understand the problems w/ HCT. Probably not! Until you truly understand what RAAS and GFR ….oh let me stop….. My message to you all non- believers. My thoughts have nothing to do with PHARMA. Keep your eyes and ears….and minds open.
HELLO, I BELEIVE TIME WILL REVEAL THAT THIS RENIN INHIBITOR WILL BE EXTREMELY EFFICACIOUS WITH FAR FEWER SIDE-EFFECTS. UNLIKE THE ACE INHIBITORS AND ANGIOTENSIN RECEPTOR BLOCKERS, A RENIN INHIBITOR PREVENTS THE RATE LIMITING STEP OF CONVERTING ANGIOTENSINOGEN TO ANGIOTENSIN I, WHICH THEN PREVENTS BOTH THE CONVERSION TO ANGIOTENSIN II, REPLACING THE ROLE OF ACE INHIBITORS, AND SECONDLY REPLACING THE NEED FOR AN ANGIOTENSIN RECEPTOR BLOCKER. SO YOU COULD REPLACE SOMEONE ON 2 DRUGS WITH ONE, OR POSSIBLY USE LOW-DOSE STRATEGIES USING ALL 3 MEDICATIONS. BY INHIBITNG A PATHWAY FURTHER UP IN A PATHWAY LEADS TO LOWER DOSES, LESS UNINTENDED SIDE EFFECTS. IN THIS CASE ULTIMATELY THE OBJECTIVE IS TO REDUCE AN OVERSTIMULATED RAAS SYSTEM, WHICH HAS MANY SIDE-EFFECTS, BY REDUCING THE OVERALL AVAILABILITY OF RENIN IN THE PLASMA AND TISSUES THIS WILL EFFECTIVELY EQUILLIBRATE THE RAAS WITHOUT HAVING TO INTERFERE WITH ANGIOTENSIN CONVERTING ENZYME ACTIVITY OR AT-1 RECEPTORS.
I have been taking Tekturna for 5 weeks — notice that I am nauseated “some times” and not others. I THOUGHT it might be
“uremia” from my CKD but I am beginning to realize that it might be the Tekturna since my kidney function numbers have not changed that much during this time. Any thoughts — I am going to stop taking it (150 mg) and see what happens. I take several other B/P drugs and do not see any difference in the numbers.
Thank you for any information you can give me. I will discuss this with my Nephrologist, as he has just started some of his patients on the drug. Also, I seem to have more problems “after” a higher fat meal. I am also an insulin dependent diabetic.
Tried Tekturna for just about 5 weeks (300mg) as 150mg did nothing to lower pressure. Dr said my body would adjust to it, but have severe dirareha each and every day while taking it. It was so bad at times that i would not go anywhere unless I knew there was a mens room nearby, Dr seemed like oh you get use to it and dismissed it, never got use to it never had real large blood pressure drop and it never lasted more then a few hours not the 24hrs they said it should.
I was having terrible headaches from the base of my neck, over the top of my head down to my left eye. I thought they were headaches and would take high doses of acetimenphen to ty and get rid of the headache. Would not go away so I do see y doctor finally. He diagnoses HBP and prescribes Tekturna. Within 24 hours the pain in my head is gone and I feel like a new person. I was irratable and was snapping at my employee’s and now I don’t feel like I did. Thank you for Tekturna. It probably saved me from a stroke or worse.
I have been taking Tekturna for 2 months in combination w/furosemide. It has kept my BP under control. I was on Lotrel, which controlled my BP but my ankles swelled to watermelon size- hence the furosemide. No side effects since starting the Tekturna, my ankles are back to normal and we’re going to try stopping the furosemide. has anyone heard any bad things about the drug?
started taking tektuna 45 days ago, 150mg seems to be working great pb is better than it as been in years, having one concern I,am coughing alot have heard of any other cases of bad coughing.
Furosemide is often used as needed for fluid retention. I’d probably look to take Lotrel and then furosemide as needed. Way cheaper than Tekturna.