Human Anti-TNFRSF10B Recombinant Antibody (TAB-203) (CAT#: TAB-203)

Wang, Liqin, et al. "cFLIP suppression and DR5 activation sensitize senescent cancer cells to senolysis." Nature Cancer 3.11 (2022): 1284-1299. https://doi.org/s43018-022-00462-2

This study investigates the effectiveness of combining cFLIP suppression and DR5 activation to target and eliminate senescent cancer cells. Utilizing CRISPR/Cas9-based genetic screens, researchers identified that senescent cells, which are resistant to apoptosis due to high cFLIP expression, can be sensitized to death by activating DR5 with an agonistic antibody. The study demonstrates that this combination treatment, enhanced by BRD2 inhibition, effectively kills senescent cells and induces a bystander effect, leading to the death of adjacent non-senescent cells in various cancer models.
Creative Biolabs significantly contributed to this research by supplying critical reagents. The agonistic antibody targeting DR5 (Cat#: TAB-203) and the BRD2 inhibitor provided by Creative Biolabs were instrumental in the study. These reagents enabled the researchers to validate the therapeutic strategy, demonstrating the potential of combining pro-senescence therapy with DR5 activation in cancer treatment.

Park, Jong-Sung, et al. "Targeting of dermal myofibroblasts through death receptor 5 arrests fibrosis in mouse models of scleroderma." Nature communications 10.1 (2019): 1128. https://doi.org/10.1038/s41467-019-09101-4

This research investigates how targeting death receptor 5 (DR5) can reverse fibrosis in scleroderma mouse models. The study reveals that scleroderma progression involves the conversion of resident fibroblasts into myofibroblasts (MFBs) expressing α-smooth muscle actin (α-SMA) with increased capacity to produce collagen and fibrogenic components. The researchers demonstrated that TLY012, an engineered human TNF-related apoptosis-inducing ligand (TRAIL), selectively blocks dermal fibroblast activation and induces DR-mediated apoptosis in α-SMA+ MFBs through upregulated DR5. Significantly, TLY012 reversed established skin fibrosis to near-normal skin architecture in both bleomycin-induced and tight skin-1 (Tsk-1) mouse models of scleroderma.
Creative Biolabs provided the anti-DR5 agonistic antibody (Conatumumab) and anti-DR4 agonistic antibody (Mapatumumab), which were used to validate the mechanism of DR-mediated apoptosis in myofibroblasts. These antibodies enabled the researchers to demonstrate that DR5, rather than DR4, is predominantly responsible for TLY012-induced apoptosis in activated myofibroblasts. This contribution was essential for establishing that targeting upregulated DR5 in α-SMA+ MFBs represents a viable therapeutic approach for fibrosis in scleroderma, potentially offering a new treatment strategy for this serious autoimmune condition.