PUMAi 

PUMAi is a PUMA inhibitor that disrupts the interaction between PUMA and BCL-xL. PUMAi inhibits apoptosis, caspase-3 activation, WNT/NOTCH pathway activation, and DNA damage. PUMAi protects intestinal tissues in mice, promotes the growth of colonoids, and reduces chemotherapy-induced weight loss, gastrointestinal damage, and lethality. PUMAi alleviates acetaminophen-induced liver injury and cytoplasmic translocation of HMGB1 in mice. PUMAi can be used in studies related to gastrointestinal injury, intestinal injury, and liver injury^[1][2][3].

PUMAi (25 μM; 15 min) inhibits the protein-protein interaction between PUMA and BCL-xL in HEK293 cell lysates, without affecting the interaction between BIM and MCL-1^[1].
PUMAi (50 μM; 24 h) protects mouse colon organoids and human primary colon organoids from CPT-induced growth inhibition, apoptosis, and WNT/Notch pathway activation^[1].
PUMAi effectively disrupts the interaction between PUMA and BCL-XL in cell-free biochemical assays^[2].

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

PUMAi (10 mg/kg; i.p.; 2 hours before each of 3 CPT-11 doses, plus 1 dose 20 hours after final CPT-11 dose) increases survival to 70% in mice with CPT-11-induced lethal gastrointestinal injury^[1].
PUMAi (10 mg/kg; i.p.; 2 hours before CPT-11) reduces LGR5⁺ intestinal stem cell apoptosis, niche cell expansion, and DNA damage in mice treated with CPT-11^[1].
PUMAi (10 mg/kg; i.p.; 2 hours before and 20 hours after each of 6 CPT-11 doses) prevents LGR5⁺ intestinal stem cell exhaustion and preserves niche integrity in mice treated with repeated doses of CPT-11^[1].
PUMAi (10 mg/kg; i.p.; 2 hours before and 20 hours after each of 6 CPT-11 doses) protects tumor-bearing mice from CPT-11-induced gastrointestinal injury and weight loss without compromising tumor response to chemotherapy^[1].
PUMAi (10 mg/kg; i.p.; 30 minutes before irradiation, 30 minutes after irradiation, and daily for 4 subsequent days) improves survival in mice with radiation-induced gastrointestinal injury^[1].
PUMAi (10 mg/kg; i.p.; single dose) administered 2 hours after acetaminophen overdose significantly reduces acetaminophen-induced liver necrosis and injury in mice, as evidenced by reduced serum ALT/AST levels, necrotic liver area, TUNEL-positive cells, and HMGB1 cytoplasmic translocation^[3].

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

403.34

C₁₉H₂₈Cl₂N₂O₃

470695-03-5

OCCN1CCN(CC(COC2=CC3=C(C=CC=C3)C=C2)O)CC1.Cl.Cl

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [1]. Yu J, et al. Method of preventing or treating treatment-induced gastrointestinal injury: US20220125746A1. 2022-04-28.

  [2]. Li M, et al. The role of P53 up-regulated modulator of apoptosis (PUMA) in ovarian development, cardiovascular and neurodegenerative diseases. Apoptosis : an international journal on programmed cell death. 2021 Jun;26(5-6):235-247.  [Content Brief]

  [3]. Chen D, et al. p53 Up-regulated Modulator of Apoptosis Induction Mediates Acetaminophen-Induced Necrosis and Liver Injury in Mice. Hepatology. 2019;69(5):2164-2179.