Being Taller with Calcineurin Inhibitors?

There are Calcineurin inhibitors available but only by prescription.

Calcineurin Inhibitors Promote Chondrogenic Marker Expression of Dedifferentiated Human Adult Chondrocytes via Stimulation of Endogenous TGFb1 Production

"Cn[Calcineurin] activity in human articular chondrocytes was significantly increased during dedifferentiation and decreased during redifferentiation in vitro. Inhibition of Cn activity by FK506 increased the expression of chondrogenic markers collagen type 2, aggrecan, and SOX9 in culture-expanded cells[So Cn inhibition stimulates chondrogenesis]. Addition of FK506{FK506Binding Protein is upregulated in LSJL} increased endogenous transforming growth factor (TGF) beta1 expression on both mRNA and protein level. The effect of FK506 on chondrogenic markers was abolished by addition of anti-TGFbeta1 antibody, indicating that the endogenous TGFbeta1 was necessary to increase chondrogenic marker expression. We also showed that chondrocyte redifferentiation by TGFbeta requires calcium influx and does not depend on changes in Cn activity. In conclusion, inhibition of Cn activity by FK506 increases the expression of chondrogenic markers via endogenous TGFbeta1 production in human articular chondrocytes. Cn inhibitors might be an alternative for the application of (recombinant) TGFbeta, to promote chondrocyte phenotype."

Of course we want to know if FK506 increases pro-chondrogenic proteins in stem cells.  It does increase TGF-Beta in a number of cell types though.

You don't want an FK506 cream as you want into directly inside the bone marrow.  The problem is calcineurin activates T cells and may have other beneficial effects.

Cytosolic free Ca2+ concentration exhibits a characteristic temporal pattern during in vitro cartilage differentiation: a possible regulatory role of calcineurin in Ca-signalling of chondrogenic cells.

"We measured changes of cytosolic Ca2+ concentration during chondrogenesis, which occurs in high-density cultures (HDC) of chondrifying chicken mesenchymal cells. A significant, transient elevation was detected in Fura-2-loaded cells on day 3 of culturing, when majority of chondrogenic cells of HDC become differentiated. This 140 nM peak of cytosolic Ca2+ concentration is a result of increased Ca-influx and is indispensable to proper chondrogenesis, because addition of 0.8mM EGTA to culture medium on day 2 or 3 significantly decreased the intracellular Ca2+ concentration abolishing the Ca2+-peak of day 3 and inhibited cartilage formation. Uncontrolled Ca2+ influx evoked by a Ca2+ ionophore exerted dual effects on chondrogenesis in a concentration-dependent manner; 0.1mg/L A23187 increased[A23187 increases calcium in intact cells so slightly more calcium than normal increased cartilage formation], whereas 5 mg/L A23187 almost totally blocked cartilage formation. Intracellular Ca-stores seemed not to have any significant participation in the regulation of changes of cytosolic Ca2+ concentration of chondrifying cells. Activity of Ca-calmodulin-dependent protein phosphatase, calcineurin responded to changes of intracellular Ca2+ concentration induced by EGTA or A23187 in a differentiation stage-dependent manner. Since inhibition of calcineurin with cyclosporine A eliminated the peak in the cytosolic Ca2+ concentration, an active regulatory role of calcineurin on Ca2+ influx of chondrifying cells can be supposed."

So calcineurin alters the Ca2+ influx of mesenchymal cells and the Ca2+ influx modifies chondrogenesis.

"[Calcineurin] is unique among phosphatases for its ability to sense changes of intracellular Ca2+ concentration through its activation by its calcium binding subunit and calmodulin"

"inhibition of calcineurin with CsA eliminates the Ca2+ peak of HDC resulting in a pronounced decrease in cartilage formation."<-So in some instances inhibiting Calcineurin will reduce height.

"the regulation of in vitro chondrogenesis is directly related to changes of cytosolic free Ca2+ concentration and calcineurin is an important signal molecule in these events"

"activity of calcineurin responds to the manipulation of intracellular Ca2+ concentration in a cell-differentiation-stage-dependent manner"

So you need Sox9 for chondrogenesis and Cn inhibition increases Sox9 but you also need an influx of calcium with Cn increases the Ca2+ peak.  Since Cn effect is linked to cell-differentiation-stage and this can be at all different stages within the growth plate, Cn inhibition is not yet a target for height growth.