BIM-23190 is a Selective SSTR2 and SSTR5 Agonist

Somatostatin (SST) is a peptide hormone, which can regulate the endocrine system. Specifically, Somatostatin affects neurotransmission and cell proliferation by interacting with G protein-coupled somatostatin receptors and inhibiting multiple releases. Besides, Somatostatin inhibits insulin and glucagon secretion. Moreover, Somatostatin is produced by neuroendocrine neurons in the hypothalamic extraperitoneal nucleus.

Somatostatin activates the 5G protein-coupled receptor family [SST receptor (SSTR)]. Furthermore, SSTRs are expressed in several human cancer cells, including neuroendocrine, gastrointestinal, pancreatic, brain, prostate, lung, and breast cancer. Meanwhile, SST indirectly regulates tumor proliferation and inhibits the release of growth hormone, growth factor, or angiogenic factor. Obviously, the antiproliferative activity of SST is related to the inhibition of adenylate cyclase and the regulation of apoptosis. Today, we will introduce a selective SSTR2 and SSTR5 agonist, BIM-23190.

BIM 23190 is a Selective SSTR2 and SSTR5 Agonist 2021 03 17 - BIM-23190 is a Selective SSTR2 and SSTR5 Agonist

BIM-23190 is a Selective SSTR2 and SSTR5 Agonist.

First of all, BIM-23190, a somatostatin analog, exhibits Ki values of 0.34 nM and 11.1 nM for SSTR2 and SSTR5, respectively. Nonetheless, BIM-23190 has the potential for the study for cancer and acromegaly.

In the second place, BIM-23190 tends to mildly stimulate PRL secretion. Importantly, BIM-23190 also reduced LI for Ki-67 and phospho-ERK1/2 and upregulated p27Kip1 expression.

Last but not the least, BIM-23190 with 50 μg/mouse for twice a day exhibits significant anti-tumor (C6 glioma) activity. Particularly, BIM-23190 inhibited in vivo C6 tumor growth, intratumoral neovessel formation. Therefore, simultaneous activation of different SSTR can inhibit the proliferation of glioma cells in vivo through direct cell inhibition and antiangiogenesis.

All in all, BIM-23190 is a selective SSTR2 and SSTR5 agonist.


Federica Barbieri, et al. Am J Physiol Endocrinol Metab. 2009 Nov;297(5):E1078-88.