Earlier I wrote that Meclizine was a very promising height growth supplement for people with open growth plates.

Here’s information on the dosages of Meclizine.  Information on the bottle should be followed.  25 to 50mg daily is what seems to be recommended.  Resistance to Meclizine may develop over time if the body begins to produce more CYP2D6.  At that point cycling would be necessary.  I can’t do research on all the possible side effects on Meclizine.  Since Meclizine is a common medication given for nausea, a doctor or pharmacist would be helpful for insight.  Especially, since it is something I just recently discovered and do not have a great deal of experience with.

Theoretically, Meclizine will only increase height in people with actively proliferating growth plate chondrocytes.  And it will only increase height in proportion to how much proliferation growth plate chondrocytes have.  So if you don’t have much natural growth left, meclizine won’t give you much growth.

Meclizine has similar effects to CNP in that both inhibit FGFR3.  However, CNP has additional effects.  For one, CNP increases levels of Guanyl Cyclase.  Since studies on Meclizine are limited, it is possible there are also as of yet unknown side effects.

Can Meclizine be absorbed and get to the growth plate chondrocytes where it exerts it’s height increasing effects by inhibiting FGFR3?

Given the below results of Meclizine being present in the serum, which would likely be delivered to growth plate chondrocytes, it is likely that yes Meclizine could indeed get to the growth plate chondrocytes.

Meclizine metabolism and pharmacokinetics: formulation on its absorption.

“the onset of action of meclizine was about 1 hour for the treatment of motion sickness and vertigo. A new suspension formulation of meclizine (MOS) was developed with the intention to achieve a rapid effect. To investigate the pharmacokinetics of the new MOS formulation versus the marketed meclizine oral tablet (MOT), a phase 1 pharmacokinetic study was performed in 20 healthy volunteers. In addition, an in vitro metabolic study using human hepatic microsome and recombinant CYP enzyme was also performed to determine the metabolic pathway in the human body. The plasma concentration of MOS appeared more rapidly in comparison to the MOT. The geometric mean ratios (90% confidence interval) of AUC(0-24) and AUC(0-∞) indicated no significant difference in bioavailability between the 2 formulations. CYP2D6 was found to be the dominant enzyme for metabolism of meclizine, and its genetic polymorphism could contribute to the large interindividual variability{So individual variations in CYP2D6 enzyme could affect the ability of meclizine to increase height in individuals with active growth plates?}.”

” In one anecdotal report, a serum level of 10 ng/mL was reported at 12 hours following an oral dose of 75 mg, and the elimination half-life of the parent compound was 6 hours. In another report, the plasma concentration-time profile of 1 subject was described, and the AUC0–24 and half-life were found to be 66.6 ng/ml·h and 7 hours, respectively. In rats, meclizine was distributed throughout most body tissues, found to cross the placenta, and metabolized in the liver to an inactive form, norchlorcyclizine. When give extravascularly, the drug is excreted in feces and urine unchanged or as metabolites such as norchlorcyclizine”<-If Meclizine is excreted or converted to the inactive form it’s not going to increase height.  However, Meclizine does seem to be present in serum and in rats was present in most body tissues

Meclizine Inhibits Mitochondrial Respiration through Direct Targeting of Cytosolic Phosphoethanolamine Metabolism.

“meclizine, an over-the-counter drug, as an inhibitor of mitochondrial respiration{Could this inhibition of mitochondrial respiration be linked to the height increase effects?}. Curiously, meclizine blunted respiration in intact cells but not in isolated mitochondria, suggesting an unorthodox mechanism. Using a metabolic profiling approach, we now show that treatment with meclizine leads to a sharp elevation of cellular phosphoethanolamine, an intermediate in the ethanolamine branch of the Kennedy pathway of phosphatidylethanolamine biosynthesis. Metabolic labeling and in vitro enzyme assays confirmed direct inhibition of the cytosolic enzyme CTP:phosphoethanolamine cytidylyltransferase (PCYT2). Inhibition of PCYT2 by meclizine led to rapid accumulation of its substrate, phosphoethanolamine, which is itself an inhibitor of mitochondrial respiration. Our work identifies the first pharmacologic inhibitor of the Kennedy pathway, demonstrates that its biosynthetic intermediate is an endogenous inhibitor of respiration. ”

They tested on fibroblasts but not on chondrocytes and stem cells.