stz

Streptozotocin (Streptozocin, NSC-85998) is an antibiotic that enters pancreatic β-cells via the glucose transporter (GLUT2) and induces DNA methylation, leading to β-cell apoptosis. It is toxic to insulin-producing cells and commonly used to establish diabetic animal models. This product is unstable in solution and is recommended to be prepared freshly before use.

Lansoprazole (A-65006) is a 2, 2, 2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a potent brain penetrant neutral sphingomyelinase (N-SMase) inhibitor (exosome inhibitor)

α-NETA is a potent choline acetyltransferase (ChA) inhibitor and an ALDH1A1 and chemokine-like receptor 1 (CMKLR1) antagonist.Anti-cancer activity,Cholinesterase and acetylcholinesterase (AChE) inhibition,Dose-dependent reduction of body weight and fasting blood glucose levels in STZ-induced diabetic mice,Significantly reduced expression of renal injury markers,May be CEP-9722 can be used for the study of diabetic nephropathy.

20-SOLA is the first water-soluble 20-HETE antagonist with oral bioavailability. It significantly improves blood pressure changes and kidney damage associated with the streptozotocin (STZ) diabetic mouse model. Additionally, 20-SOLA acts as a GPR75 receptor blocker. This compound is useful in research related to cardiovascular pathology.

eeAChE-IN-3 (compound YS3g) is an orally bioavailable and potent inhibitor of EeAChE and IL-6, with IC50 values of 0.54 μM for EeAChE, 0.49 μM for RatAChE, 8.54 μM for RatBuChE, and 0.57 μM for IL-6. It can enhance learning and memory deficits in mice induced by STZ (streptozotocin) and shows potential for Alzheimer's disease (AD) research.

7,4'-Dimethoxy-3-hydroxyflavone is an orally active PAR4 antagonist. This compound inhibits PAR4-mediated human platelet aggregation with an IC50 of 1.4 μM. It disrupts PAR4-mediated aggregation and related signaling pathways, including NF-κB, Ca2+/protein kinase C (PKC), Akt, ERK, and p38. In a streptozotocin (STZ)-induced diabetic mouse model, 7,4'-Dimethoxy-3-hydroxyflavone inhibits vascular PAR4 expression, improves endothelial dysfunction, and reduces oxidative stress. Additionally, it prevents thrombosis in mice without affecting bleeding time.

TFSeB is a neuroprotective agent. It reduces STZ-induced MAO-B and AChE activity. TFSeB exerts its neuroprotective effects by increasing the expression of BCL-2, BDNF, and NRF2, while decreasing BAX expression. It also reduces lipid peroxidation (TBARS) and reactive oxygen species (ROS) levels. Additionally, TFSeB alleviates neuroinflammation and is applicable in Alzheimer's disease research.

GLUT4 activator3 (Compound 13a) is an antidiabetic agent that targets GLUT4 translocation in skeletal muscle. It facilitates the translocation of glucose transporter 4 (GLUT4) within skeletal muscle cells and effectively reduces blood glucose levels in diabetic rats induced by STZ.

DPP-4-IN-17 is an orally active and selective inhibitor of dipeptidyl peptidase-4 (DPP-4) with an IC50 value of 0.12 nM. It increases the enzyme's Km value (75.73 μM compared to the substrate alone at 27.18 μM) and reduces catalytic efficiency. In Streptozotocin (STZ)/Nicotinamide (NA)-induced diabetic rats, DPP-4-IN-17 lowers blood glucose levels and reverses weight loss. This compound is useful for research in type 2 diabetes (T2DM).

CLP290 is an activator of the neuron-specific K+-Cl cotransporter KCC2 and displays potential for the treatment of a wide range of neurological and psychiatric indications.

Y13g is a potent inhibitor of Interleukin-6 (IL-6) and acetylcholinesterase (AChE), both significant targets in Alzheimer's Disease (AD) progression. Y13g reverses memory deficits induced by STZ and demonstrates histopathology similar to that of normal animals [1].

Y13g dihydrochloride is a potent inhibitor of interleukin 6 (IL-6) and acetylcholinesterase (AChE) (both targets of Alzheimer's disease (AD) progression are related). Y13g dihydrochloride reverses STZ-induced memory deficits and exhibits histopathology similar to normal animals.

Vin-C01 can be used for the research of type 2 diabetes mellitus that is a potent protective agent of pancreatic β-cells (EC 50 = 0.22 μM). Vin-C01 effectively protects β-cells from apoptosis induced by STZ and promotes β-cell survival [1].

Vin-F03 can be used in the research of type 2 diabetes mellitus that is an effective protective agent of pancreatic β-cells (EC50 = 0.27 μM). Vin-F03 potently promotes the survival of β-cell and protects β-cells from apoptosis induced by STZ[1].

Gliclazide-d4 is intended for use as an internal standard for the quantification of gliclazide by GC- or LC-MS. Gliclazide is a sulfonylurea and an inhibitor of pancreatic β-cell ATP-sensitive potassium (KATP) channels. It is selective for pancreatic β-cell over cardiac and arterial smooth muscle cell KATP channels. Gliclazide (5 μM) increases insulin-induced glucose uptake and glucose transporter 4 (GLUT4) translocation to the plasma membrane in a differentiated 3T3L1 adipocyte model of insulin resistance induced by hydrogen peroxide. Gliclazide (5 and 10 μg/ml) reduces LDL oxidation by human aortic smooth muscle cells (HASMCs), decreasing TBARS content and 8-isoprostane levels. It also decreases oxidized LDL-induced HASMC proliferation and monocyte adhesion when used at concentrations ranging from 1 to 10 μg/ml. Gliclazide (5 mg/kg) reduces serum glucose levels and increases glucose uptake by isolated rat hindquarters in a model of diabetes induced by streptozotocin (STZ).

BBT has anti-hyperglycemic activity, acting through cAMP/PKA and the persistent L-type voltage-dependent Ca2+ channels/CaMK2 pathways to protect β-cells from cytokine or streptozotocin (STZ)-induced cell death and restore β-cell function, used in studies of diabetes.

R 715, a bradykinin B1 receptor antagonist, inhibits contractions in isolated human umbilical cords that express bradykinin B1 receptors (pA2 = 8.49). When administered at doses of 200, 400, and 600 µg/kg, R 715 enhances latency to tail withdrawal in the tail-flick test for diabetic neuropathy mouse models induced by streptozotocin (STZ), signaling potential analgesic properties. Furthermore, at a 1 mg/kg per day dosage, it mitigates symptoms in a mouse model of experimental autoimmune encephalomyelitis (EAE) induced by MOG35-55 antigen peptide, such as reducing hind limb weakness and paralysis, improving gait symmetry, and decreasing spinal inflammation, neuron demyelination, and lesion monocyte invasion. Additionally, R 715 at 0.01 nmol/animal, administered intracerebroventricularly (i.c.v.), lowers mean arterial blood pressure and increases heart rate in spontaneously hypertensive rats, indicating cardiovascular effects.

Ficusin has antioxidant, antilipidemic and antidiabetic effects, it can lower the levels of fasting blood glucose, plasma insulin, body weight gain in HFD-STZ induced diabetic rats, and can significantly enhance the PPARγ expression and improve the transl

Serpentine is an alkaloid found in the roots of Rosa Centifolia that acts as an insulin sensitizer to assist insulin in lowering blood glucose.Serpentine activates the phosphorylation of AMPK, which stimulates glucose uptake by C2C12 cells.Serpentine increases the expression of GSK-3β mRNA in muscle tissues, which enhances glucose uptake.Serpentine also increases glucose production and hepatic gluconeogenesis.Serpentine has a significant effect on glucagon secretion and hepatic gluconeogenesis. Serpentine significantly increased glucagon secretion and hepatic gluconeogenesis. In high-fat diet/streptozotocin (HFD/STZ)-induced diabetic mice, Serpentine significantly prolonged insulin hypoglycemia, significantly decreased exogenous insulin use, and inhibited endogenous insulin secretion.

Cenupatide is a urokinase plasminogen activator receptor (uPAR) inhibitor. Cenupatide inhibits uPAR binding to the formyl peptide receptors (FPRs) can improve kidney lesions in a rat model of STZ-induced diabetes. Cenupatide reverted STZ-induced up-regula