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GENE:

SPR (Sepiapterin Reductase)

i
Other names: SPR, Sepiapterin Reductase, SDR38C1, Sepiapterin Reductase (7,8-Dihydrobiopterin:NADP+ Oxidoreductase), Sepiapterin Reductase (L-Erythro-7,8-Dihydrobiopterin Forming), Short Chain Dehydrogenase/Reductase Family 38C, Member 1
Associations
Trials
3ms
Isorhamnetin attenuates renal interstitial fibrosis by targeting TWEAK/Fn14-mediated epithelial-mesenchymal transition. (PubMed, Front Immunol)
Overexpression of Fn14 counteracts the renoprotective effects of ISO, mitigating its influence on the inactivation of the TWEAK/Fn14 signaling pathway. These confirmed that ISO inhibits the EMT of renal tubular epithelial cells by suppressing the TWEAK/Fn14 signaling pathway.
Journal
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TNFA (Tumor Necrosis Factor-Alpha) • CDH1 (Cadherin 1) • TGFB1 (Transforming Growth Factor Beta 1) • SPR (Sepiapterin Reductase)
3ms
Comparative insight: hereditary colorectal cancer registries in Iran, Singapore, and South Africa. (PubMed, Fam Cancer)
The registries' combined experiences underscore the critical need for integrated, culturally sensitive strategies combining genetic testing, enhanced surveillance, and family-based management to improve outcomes for individuals and families affected by hereditary CRC. Future efforts should focus on addressing disparities in access to care and expanding research to improve understanding and management of this complex disease.
Clinical • Journal
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SPR (Sepiapterin Reductase)
almost2years
Trial completion
|
SPR (Sepiapterin Reductase)
over2years
HRA00129-C004, a Novel c-Met ADC with Promising Preclinical Anti-tumor Activity and Expanded Therapeutic Window (IASLC-WCLC 2023)
Telisotuzumab vedotin (Teliso-V) is a c-Met ADC, which composed of a c-Met antibody (ABT-700) and a microtubule inhibitor MMAE... In summary, HRA00129-C004 is a novel c-Met targeted ADC with a highly permeable payload demonstrating great stability and anti-tumor activity in both in vitro and in vivo. The promising preclinical data support advancing HRA00129-C004 into clinical testing, and Investigational New Drug (IND) application to NMPA has been submitted.
Preclinical
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EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase) • SPR (Sepiapterin Reductase)
|
EGFR wild-type • EGFR overexpression • MET overexpression • MET expression
|
Emrelis (telisotuzumab vedotin-tllv)
over2years
HRA00129-C004, a Novel c-Met ADC with Promising Preclinical Anti-tumor Activity and Expanded Therapeutic Window (IASLC-WCLC 2023)
Telisotuzumab vedotin (Teliso-V) is a c-Met ADC, which composed of a c-Met antibody (ABT-700) and a microtubule inhibitor MMAE... In summary, HRA00129-C004 is a novel c-Met targeted ADC with a highly permeable payload demonstrating great stability and anti-tumor activity in both in vitro and in vivo. The promising preclinical data support advancing HRA00129-C004 into clinical testing, and Investigational New Drug (IND) application to NMPA has been submitted.
Preclinical
|
EGFR (Epidermal growth factor receptor) • MET (MET proto-oncogene, receptor tyrosine kinase) • SPR (Sepiapterin Reductase)
|
EGFR wild-type • EGFR overexpression • MET overexpression • MET expression
|
Emrelis (telisotuzumab vedotin-tllv)
almost3years
Ninety-six-hour starved peripheral blood mononuclear cell supernatant inhibited LA7 breast cancer stem cells induced tumor via reduction in angiogenesis and alternations in Gch1 and Spr expressions. (PubMed, Front Immunol)
This phenomenon could be mediated through direct cytotoxic effects, inhibition of cell proliferation and migration in association with reduction in Gch1 and Spr genes expression, angiogenesis and mitosis rate, and necrosis augmentation. The preliminary data obtained from the present study need to be investigated on a larger scale and can be used as a pilot for further studies on the biology of cancer development.
Journal • Cancer stem
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SOX2 • POU5F1 (POU Class 5 Homeobox 1) • GCH1 (GTP Cyclohydrolase 1) • SPR (Sepiapterin Reductase)
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SOX2 expression • POU5F1 expression
almost3years
Blockade of NMT1 enzymatic activity inhibits N-myristoylation of VILIP3 protein and suppresses liver cancer progression. (PubMed, Signal Transduct Target Ther)
Mechanistically, desloratadine binds to Asn-246 in NMT1 and inhibits its enzymatic activity, disrupting the NMT1-mediated myristoylation of the VILIP3 protein and subsequent NFκB/Bcl-2 signaling. Conclusively, this study demonstrates that desloratadine may be a novel anticancer drug and that NMT1-mediated myristoylation contributes to HCC progression and is a potential biomarker and therapeutic target in HCC.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • SPR (Sepiapterin Reductase)