8-Bromo-cAMP sodium salt (8-Br-Camp sodium salt) is a long-acting derivative of cyclic AMP. It is an activator of cyclic AMP-dependent protein kinase（PKA）, but resistant to degradation by cyclic AMP phosphodiesterase.

PKA:0.05 μM(Ka)

METHODS: Endothelial HUVECs were treated with 8-Bromo-cAMP sodium salt (100 µM) for 3 h. Cell migration was detected by Boyden Chamber assay.
RESULTS: Increased cell migration was observed when conditioned media from MC3T3-E1 cells exposed to 8-Bromo-cAMP was supplemented with HUVECs. In contrast, conditioned medium from control untreated cells lacked this activity. [1]
METHODS: The leukemia cell line AML193 was treated with 8-Bromo-cAMP sodium salt (1 mM) or IL-3 (500 ng/mL) for 1-15 min, and target protein expression levels were detected by Western Blot.
RESULTS: In growth-arrested AML193 cells, the maximal effect of IL-3 on Erk1,2 phosphorylation was time-dependent and occurred within a time window of 5-15 min after the addition of growth factors. 8-Bromo-cAMP also induced Erk1,2 phosphorylation in these cells, with a maximal stimulation observable between 1-5 min. [2]

METHODS: To evaluate the effect of cAMP/PCA on angiogenesis and VM in CRC cells, 8-Bromo-cAMP sodium salt (60 mg/kg) was intraperitoneally injected into BALB/c mice bearing CT26 tumor tissues once a day for seven days.
RESULTS: 8-Bromo-cAMP treatment significantly reduced the number of tumors. 8-Bromo-cAMP treatment inhibited angiogenesis and VM. 8-Bromo-cAMP acted through the cAMP/PKA-ERK pathway and EMT process in CRC. [3]