8-Br-ADPR disodium  (Synonyms: 8-Bromoadenosine-5'-O-diphosphoribose disodium)

8-Br-ADPR disodium (8-Bromoadenosine-5'-O-diphosphoribose) is a TRPM2 inhibitor and ADPR signaling pathway antagonist. 8-Br-ADPR disodium inhibits glucagon-mediated nuclear calcium signaling and downstream CaMKII/CREB phosphorylation by blocking ADPR-induced TRPM2 activation. 8-Br-ADPR disodium significantly reduces gluconeogenic gene expression and blood glucose levels in diabetic models. 8-Br-ADPR disodium effectively blocks ADPR-mediated calcium signal transduction in NK cells, inhibits immune synapse formation, granzyme B release and cytolytic activity against melanoma cells. 8-Br-ADPR disodium is widely used in studies related to diseases such as diabetes, melanoma and lymphoma^[1][2].

8-Br-ADPR (100 μM; preincubated prior to glucagon treatment) disodium specifically blocks glucagon-induced sustained nuclear calcium signals in mouse primary hepatocytes, without altering cytosolic calcium signals^[1].
8-Br-ADPR (100 μM; 30 min preincubated before ADPR treatment) disodium completely blocks ADPR-induced calcium flux between the perinuclear space and nucleoplasm in isolated nuclei from mouse primary hepatocytes^[1].
8-Br-ADPR (100 μM; 30 min preincubated before 100 nM glucagon treatment for 4 h) disodium significantly reduces glucagon-induced G6pc and Pck1 mRNA expression in mouse primary hepatocytes^[1].
8-Br-ADPR (100 μM; 20 min) disodium inhibits B16F10-induced translocation of perforin and granzyme B to the immunological synapse in murine NK cells^[2].
8-Br-ADPR (100 μM; 20 min) disodium reduces the cytolytic activity of murine NK cells against B16F10 melanoma target cells^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

8-Br-ADPR (32 mg/kg; i.v.; single dose) disodium reduces fasting and pyruvate-induced blood glucose levels in wild-type mice by inhibiting hepatic gluconeogenic gene expression and CRE-mediated transcriptional activity^[1].
8-Br-ADPR (32 mg/kg; i.v.; single dose) disodium reduces pyruvate-induced blood glucose levels in diabetic db/db mice by inhibiting hepatic gluconeogenic gene expression and CRE-mediated transcriptional activity^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

682.18

C₁₅H₂₀BrN₅Na₂O₁₄P₂

Solid

O[C@H]1[C@@H](O)[C@H](N2C(Br)=NC3=C2N=CN=C3N)O[C@@H]1COP(OP(OC[C@H]4OC(O)[C@H](O)[C@@H]4O)(O[Na])=O)(O[Na])=O

Room temperature in continental US; may vary elsewhere.

-20°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

• [1]. Rah SY, et al. CD38/ADP-ribose/TRPM2-mediated nuclear Ca²⁺ signaling is essential for hepatic gluconeogenesis in fasting and diabetes. Exp Mol Med. 2023;55(7):1492-1505.  [Content Brief]

  [2]. Rah S Y, et al. ADP-ribose/TRPM2-mediated Ca2+ signaling is essential for cytolytic degranulation and antitumor activity of natural killer cells[J]. Scientific reports, 2015, 5(1): 9482.