3 Results for "

Bcl-xL mRNA

" in MedChemExpress (MCE) Product Catalog:
Products (3)

3 Results for "Bcl-xL mRNA" in MCE Product Catalog:

Cat. No.: HY-170935
Research Areas:  

Cancer

SRSF1-IN-1 is a SRSF1 inhibitor. SRSF1-IN-1 inhibits SRSF1 expression, thereby modulating the splicing of Bcl-x pre-mRNA. SRSF1-IN-1 inhibits the proliferation of various cancer cells. SRSF1-IN-1 induces apoptosis in gastric cancer cells, reduces Bcl-xl expression, and upregulates cleaved PARP and caspase 3. SRSF1-IN-1 induces autophagy and promotes cell death. SRSF1-IN-1 exhibits anti-tumor activity in a mouse gastric cancer xenograft model. SRSF1-IN-1 can be used for the research of various cancers including liver cancer, gastric cancer, breast cancer, colon cancer, glioma, and melanoma .
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Cat. No.: HY-188136
Research Areas:  

Cancer

ASO-4625 is a 20-nucleotide gapmer antisense oligonucleotide with a full phosphorothioate backbone and 2'-O-(2-methoxy) ethyl ribose modifications, which targets BCL2 mRNA and BCL2L1 mRNA. ASO-4625 downregulates Bcl-2 expression via an RNase H-dependent antisense mechanism with 100% complementarity, and downregulates Bcl-xL expression via the same mechanism with three mismatches. ASO-4625 induces Apoptosis and acts as a chemosensitizer. ASO-4625 does not significantly modulate the expression of Bcl-W, survivin, Akt, or p53 mRNA. ASO-4625 can be used in studies of breast cancer and non-small cell lung cancer .
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Cat. No.: HY-188137
Research Areas:  

Cancer

ASO-5005 is a 20-mer Gapmer antisense oligonucleotide modified with locked nucleic acids (LNA), featuring a full phosphorothioate backbone, which targets BCL2 mRNA and BCL2L1 mRNA. ASO-5005 downregulates Bcl-2 expression via an RNase H-dependent mechanism, with its sequence fully complementary to BCL2 mRNA; it simultaneously downregulates Bcl-xL expression via an RNase H-dependent mechanism, with three mismatches between its sequence and BCL2L1 mRNA, while LNA modification enhances its activity against this mismatched target. ASO-5005 induces Apoptosis by activating Caspase-3 and cleaving ICAD. ASO-5005 does not significantly regulate the expression of Bcl-W, Survivin, Akt, or p53 in tumor cells. ASO-5005 can be used for research on breast cancer and non-small cell lung cancer .
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