Melanocortin (MC) 3-MSH (Melanocyte-Stimulating Hormone) is believed to signal through the MC 3 receptor. It induces a sustained increase in intracellular free calcium levels ([Ca2+]i) in a subpopulation of pituitary cells. Most of the cells responding to 3-MSH express more than one pituitary hormone mRNA. The effect of 3-MSH is blocked by SHU9119, a MC3R and MC4R antagonist, in only 50% of the responsive cells, suggesting that in half of these cells the mediating receptor is not the MC3R. Low picomolar doses of 3-MSH increase [Ca2+]i in the growth hormone (GH)- and prolactin (PRL)-secreting GH3 cell line.

The impact of spleen tyrosine kinase (Syk) signaling might be prominent in lupus because (i) Syk is a shared downstream signaling molecule among circulating immune complex, LPS, and (1→3)-β-D-glucan (BG), and (ii) all of these factors are detectable in the serum of Fc gamma receptor IIb-deficient (FcgRIIb-/-) mice with sepsis. Syk inhibition downregulated several inflammatory pathways in FcgRIIb-/- macrophages activated with BG + LPS suggesting the potential anti-inflammatory impact of Syk inhibitors in lupus.

Physalin A exerts anti-tumor activity in non-small cell lung cancer cell lines by suppressing JAK/STAT3 signaling, it inhibits androgen-independent prostate cancer cell growth through activation of cell apoptosis and downregulation of androgen receptor expression.