View Full Version : Focalin & Focalin XR

05-22-10, 12:05 PM
Am an Adult female, just started focalin & XR 2 weeks ago
This morning at 3am 5mg focalin 7:30 am took 10mg focalin xr
it is now 10:30 am & I feel totally whipped out, no energy & tired as all hey.
Was on 100mg Strattera up until about 2 weeks ago. Really liked it no problems just seemed to stop working. I have had a headache everyday since starting this stuff. Does it take awhile before it starts working? I wish the strattera wouldnt have stopped.

05-24-10, 06:45 AM
Typically stimulants work from day 1 unless the dosage is incorrect. To me it sounds like you need a higher dose. Focalin XR goes all the way up to 30mg now so that gives you a lot of room.

05-27-10, 07:00 AM
Switch to focalin IR only. and see how it works out.

focalin XR. kicks in twice

half instantly and the other 4 hours later

so you might have a crash after 3 hours of focalin XR then an hour later feel the second dose of the XR kicks in. plus XR is affected by stomach conditions.

if you take too much of focalin you will feel sedated/dizzy and then agitated (my experience)

focalin is very potent (new studies show that it is 3 times more potent than Ritalin) not just twice as commonly known.

05-27-10, 07:45 AM
FOUR hours??? That explains why I feel like it stops working before dinnertime. I'm liking it so far, although I'm feeling like 10 mg is a little too low, also, but I knew it was pooping out a lot faster than Adderall xr used to.

According to my doctor, 10 mg is the starting dose. Doctors like to start you on a low dose because if you have a bad reaction, it's because of the medication itself, not because the dose was too high. It's better to see if the effect is positive and the side effects are bearable and work your way up than to start off high and have the sudden reaction to that dose make you decide to abandon the medication entirely.

Coming off a stimulant at a dose that worked for you and switching to one that's a lower dose quite possibly is why you feel tired, as JR1973 said. Depending on the medication, the standard is two to four weeks on a dosage before increasing it.

05-27-10, 09:11 AM
thats true. 10 mg is the starting dose.

But I used to take focalin before then switched to adderall brand by shire (old formula) which was even better. after they changed adderall brand formula went down hill from there. tried barr which was exactly the same as the new brand. then corepharma which is garbage (my personal experience). then finally settled on sandoz. sandoz is the best available but its mild and does not have that motivational and focus kick for my inattentive ADHD. plus made me hyperfocus and lazy for some reason.

after switching back to focalin. it took two weeks for me to get used to focalin because its a step down from ampthamine. but it was an excellent decision. after two weeks i felt great. i take brand by novartis so quality is there, feel it when its working, adderall works when it wants, last shorter than adderall so i can tailor it much more effectively to my daily schedule. plus i sleep much better when it wears off. adderall fell short when i needed it the most during the day but was always lingering in the background when i wanted to go to sleep. and the final advantage it causes less down regulation of dopamine receptors after chronic use unlike amphetamines which has more neurotoxin effects on dopamine receptors.

ritalin / focalin were actually developed as a better alternative to amphetamines which was widely used in the 50s (it was an OTC)

focalin is even more refined form of ritalin
dex-methylphen (foc)
ritalin is dex+ levo methylphen

many studies found that dex-methylphen is responsible for the adhd effects in ritalin. and that the levo-part is
useless for adhd (more for antidepressant)
found also that the levo part might impede the function of the dex part. with the levo removed like in focalin
the dex is even more effective and more potent
which explains new finding that focalin is more than 3 times potent as ritalin.

IRs are generally stronger than the XR. because not all of the XR beads react and just pass without releasing the active ingredient. just like you cant get all the ketchup from the bottle or have a 100% efficient heat engine

but the IR is readily available and do not require an extra step to release the active ingredient. And the XRs are like a million dollars for one month prescription

Differential pharmacokinetics and pharmacodynamics of methylphenidate enantiomers: does chirality matter?


d,l-threo-methylphenidate (MPH) Ritalin is an effective first-line treatment for the symptoms associated with attention-deficit/hyperactivity disorder. threo-methylphenidate inhibits the dopamine transporter and the norepinephrine transporter, resulting in elevations of these monoamines after impulse release.

Although MPH has long been administered as a racemic mixture of the 2 enantiomers, d-MPH and l-MPH, converging lines of evidence drawn from investigations using in vitro systems, animal models, and humans indicate that it is predominantly, if not exclusively, d-MPH that mediates the pharmacological/therapeutic actions of MPH.

In both rodent and primate animal models, the binding of radiolabeled d-MPH to dopamine transporter was found to be selective, saturable, and reversible, whereas binding of l-MPH was diffuse and nonspecific. The behavioral effects of the enantiomers of MPH have been tested in several animal models,

and results indicate these observed behavioral changes are likewise mediated by d-MPH, whereas l-MPH has little or no effect.

The contribution of the l-isomer to the overall pharmacological profile of the racemate remains unclear, owing to several studies suggesting that l-MPH may not be merely an inert isomeric ballast.

For example, behavioral studies conducted in rats demonstrate an attenuation (weakening) of the effect of d-MPH in animals pretreated with l-MPH,

suggesting that l-MPH may interfere with the action of the active enantiomer (d-amp). The importance of MPH chirality to central nervous system MPH receptor targeting has culminated in human

imaging studies revealing that d-MPH binds specifically to striatal structures, whereas l-MPH binding is nonspecific.

Taken together, data from in vitro, animal, and human studies support the premise that the d-enantiomer of MPH mediates the neurophysiological actions of MPH and therefore likely mediates its clinical efficacy.

Look at page 64 of the below link. it shows a PET image of the brain after focalin ingestion vs after ritalin ingestion

showing parts of the brain having higher activity while on focalin.

the file has interesting facts about how diff release tech work in adhd meds

ritalin LA and focalin XR use the same sodas tech

05-27-10, 12:58 PM
Im now building back up my 100 mg strattera turns out didnt know i could take both dr figures my medicine probably just needs tweaked. So now Im
taking 5mg focalin @2:30 am & focalin xr 10mg, 20mg lexapro, @ 6:00pm
I take 40mg strattera. The strattera really does help with the memory.. thanks for the help

06-03-10, 10:03 PM
Focalin is now suggested as being 3 x more potent than
regular Ritalin? I would like to see the evidence, that would be killer. Focalin is the bomb!

06-04-10, 09:32 AM
d-methylphen is focalin

dl-methyphen is ritalin

"RESULTS: l-Methylphenidate did not affect locomotor activity in either lesioned rats or controls. d-Methylphenidate (ED(50)=1.66 mg/kg) was 3.3 times more potent than dl-methylphenidate (ED(50)=5.45 mg/kg) in reducing locomotor hyperactivity in lesioned rats.

In addition, pretreatment of lesioned rats with l-methylphenidate significantly reduced the motor inhibiting effects of d-methylphenidate.

CONCLUSIONS: The more active enantiomer, as predicted, was d-methylphenidate, but the l-enantiomer interfered with its effects, suggesting that clinical potency of d-methylphenidate may be more than twice that of the racemate.

Stereoselective effects of methylphenidate on motor hyperactivity in juvenile rats induced by neonatal 6-hydroxydopamine lesioning.

Davids E (, Zhang K (, Tarazi FI (, Baldessarini RJ (
Department of Psychiatry & Neuroscience Program, Harvard Medical School and Mailman Research Center, McLean Division of Massachusetts General Hospital, Belmont, MA 02478, USA.