ADH-1 trifluoroacetate is an N-cadherin antagonist, which inhibits N-cadherin mediated cell adhesion.
体外研究 (In Vitro)
ADH-1 (0.2 mg/mL) blocks collagen I-mediated changes in pancreatic cancer cells, and is highly effective at preventing cell motility that is induced by expression of N-cadherin. ADH-1 (0, 0.1, 0.2, 0.5 and 1.0 mg/mL) induces apoptosis in a dose-dependent and N-cadherin-dependent manner[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
ADH-1 (50 mg/kg) significantly prevents tumor growth and metastasis in a mouse model for pancreatic cancer. ADH-1 prevents tumor cell invasion and metastasis in an orthotopic model for pancreatic cancer using N-cadherin overexpressing BxPC-3 cells[1]. ADH-1, at the dosages evaluated, does not display either antiangiogenic activity in a rat aortic ring assay or antitumor potential in a PC3 subcutaneous xenograft tumor model[2]. ADH-1 (10 mL/kg, i.p.) augmentation of melanoma tumor growth is overcome through its ability to make regionally infused melphalan more effective. ADH-1 mediated augmentation of melanoma tumor growth is not altered by regionally infused temozolomide. In A375, but not DM443 xenografts, ADH-1 treatment increases phosphorylation of AKT at serine 473. ADH-1 slightly diminishes N-cadherin expression in both xenografts[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
684.71
Formula
C24H35F3N8O8S2
CAS 号
1135237-88-5
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Shintani Y, et al. ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. Int J Cancer. 2008 Jan 1;122(1):71-7.
[2]. Li H, et al. ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs. 2007 Jun;18(5):563-8.
[3]. Turley RS, et al. Targeting N-cadherin increases vascular permeability and differentially activates AKT in melanoma. Ann Surg. 2015 Feb;261(2):368-77
Animal Administration [1]
Animals are anesthetized, and 40 μL of a single cell suspension containing 50,000 cells is injected into the pancreas. Mice are randomized into treatment groups 10 days after surgery. For treatment, mice are injected intraperitoneally once per day with ADH-1 at 50 mg/kg in 100 μL PBS (×1 per day, ×5 per week for 4 weeks). For in vivo bioluminescence, D-Luciferin is administered by intraperitoneal injection. Data are acquired 20 min after injection using the IVIS system. Tumor growth is monitored every 10 days from day 10 to day 50 after surgery. Luciferase activity is quantified using the IVIS system. Two months after surgery, the mice are killed, and the pancreas, liver, lung, and disseminated nodules are harvested, fixed in 10% buffered formalin, and embedded in paraffin. Serial 5-μM sections are cut, mounted on slides, and stained with HE using standard procedures. Sections are also stained for TUNEL. Sections are examined using a Zeiss Axioscop 40 microscope equipped with an AxioCam MR digital camera and software.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Shintani Y, et al. ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. Int J Cancer. 2008 Jan 1;122(1):71-7.
[2]. Li H, et al. ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs. 2007 Jun;18(5):563-8.
[3]. Turley RS, et al. Targeting N-cadherin increases vascular permeability and differentially activates AKT in melanoma. Ann Surg. 2015 Feb;261(2):368-77
ADH-1, an N-cadherin antagonist, inhibits N-cadherin mediated cell adhesion.
体外研究 (In Vitro)
ADH-1 (0.2 mg/mL) blocks collagen I-mediated changes in pancreatic cancer cells, and is highly effective at preventing cell motility that is induced by expression of N-cadherin. ADH-1 (0, 0.1, 0.2, 0.5 and 1.0 mg/mL) induces apoptosis in a dose-dependent and N-cadherin-dependent manner[1].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
ADH-1 (50 mg/kg) significantly prevents tumor growth and metastasis in a mouse model for pancreatic cancer. ADH-1 prevents tumor cell invasion and metastasis in an orthotopic model for pancreatic cancer using N-cadherin overexpressing BxPC-3 cells[1]. ADH-1, at the dosages evaluated, does not display either antiangiogenic activity in a rat aortic ring assay or antitumor potential in a PC3 subcutaneous xenograft tumor model[2]. ADH-1 (10 mL/kg, i.p.) augmentation of melanoma tumor growth is overcome through its ability to make regionally infused melphalan more effective. ADH-1 mediated augmentation of melanoma tumor growth is not altered by regionally infused temozolomide. In A375, but not DM443 xenografts, ADH-1 treatment increases phosphorylation of AKT at serine 473. ADH-1 slightly diminishes N-cadherin expression in both xenografts[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
570.69
Formula
C22H34N8O6S2
CAS 号
229971-81-7
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Shintani Y, et al. ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. Int J Cancer. 2008 Jan 1;122(1):71-7.
[2]. Li H, et al. ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs. 2007 Jun;18(5):563-8.
[3]. Turley RS, et al. Targeting N-cadherin increases vascular permeability and differentially activates AKT in melanoma. Ann Surg. 2015 Feb;261(2):368-77
Animal Administration [1]
Animals are anesthetized, and 40 μL of a single cell suspension containing 50,000 cells is injected into the pancreas. Mice are randomized into treatment groups 10 days after surgery. For treatment, mice are injected intraperitoneally once per day with ADH-1 at 50 mg/kg in 100 μL PBS (×1 per day, ×5 per week for 4 weeks). For in vivo bioluminescence, D-Luciferin is administered by intraperitoneal injection. Data are acquired 20 min after injection using the IVIS system. Tumor growth is monitored every 10 days from day 10 to day 50 after surgery. Luciferase activity is quantified using the IVIS system. Two months after surgery, the mice are killed, and the pancreas, liver, lung, and disseminated nodules are harvested, fixed in 10% buffered formalin, and embedded in paraffin. Serial 5-μM sections are cut, mounted on slides, and stained with HE using standard procedures. Sections are also stained for TUNEL. Sections are examined using a Zeiss Axioscop 40 microscope equipped with an AxioCam MR digital camera and software.
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Shintani Y, et al. ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. Int J Cancer. 2008 Jan 1;122(1):71-7.
[2]. Li H, et al. ADH1, an N-cadherin inhibitor, evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs. 2007 Jun;18(5):563-8.
[3]. Turley RS, et al. Targeting N-cadherin increases vascular permeability and differentially activates AKT in melanoma. Ann Surg. 2015 Feb;261(2):368-77