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7 results about "Damage dna" patented technology

Intervertebral disc degeneration therapeutic agent containing stem cell-derived extracellular vesicles and method of preparing the same

PendingCN122624528ATissue repairUmbilical cord
The curcumin-coupled copper-gold bimetallic nanoszyme AuCu-Cur prepared by the application can remove ROS and relieve oxidative stress, prevent further damage to DNA, and introduce human umbilical cord mesenchymal stem cell-derived extracellular vesicles (hUCMSC-EVs) to improve the bioavailability. In the system, curcumin can repair damaged DNA by promoting the expression of NEIL3. In addition, the vesicles themselves are rich in various tissue repair-related proteins and RNAs, which can promote DNA replication of notochordal cells (NPCs), reverse the aging state and stimulate extracellular matrix synthesis. In the IVDD model induced by rat tail vertebra puncture, we confirmed that the material has strong antioxidant and DNA repair capacity and can effectively delay cell aging, thereby relieving the progression of IVDD. Compared with existing intervertebral disc biomaterial treatments, the present scheme can realize continuous DNA repair, which is an active, multi-target repair program that not only interrupts the vicious cycle of intervertebral disc degeneration but also promotes tissue transformation to regeneration.
Owner:XIEHE HOSPITAL ATTACHED TO TONGJI MEDICAL COLLEGE HUAZHONG SCI & TECH UNIV

Damaged DNA repairing composition including GABA as active ingredient

[Problem] To provide a composition for a supplement, medicine, food or drink, feed, or similar that is capable of repairing damaged DNA. [Solution] This damaged DNA repairing composition that is characterized by including GABA as an active ingredient can be used as a highly safe supplement, medicine, food or drink, or feed, for anti-aging or health maintenance.
Owner:SANWA SHURUI

Azido modified platinum radiotherapy sensitizer as well as preparation method and application thereof

The invention discloses an azide modified platinum radiotherapy sensitizer as well as a preparation method and application thereof. The azide modified platinum radiotherapy sensitizer is an azide modified platinum complex, comprises a cis platinum complex and a trans platinum complex, and is characterized in that the structure of the azide modified platinum radiotherapy sensitizer is shown in the specification; in the formula I, R1 is cyclohexylamine or 2-methylpyridine; in the formula II, R2 is ammonia molecules or pyridine. The azide modified platinum radiotherapy sensitizer can generate a platinum-nitrogen-bin free radical under the irradiation of X rays, and by utilizing a nitrogen transfer reaction in organic chemistry, the platinum-nitrogen-bin free radical generated after the compound is irradiated by rays can be covalently coupled with some DNA (Deoxyribose Nucleic Acid) or protein, so that the sensitivity of the radiotherapy sensitizer is improved. The radiotherapy sensitization effect in tumor radiotherapy is achieved by directly damaging DNA and hindering DNA repair.
Owner:UNIV OF SCI & TECH OF CHINA

Platinum anti-tumor conjugate as well as preparation method and application thereof

The invention discloses a platinum anti-tumor conjugate and a preparation method and application thereof.The conjugate is reduced into a bivalent platinum drug and an LOXL2 inhibitor in tumor cells, the bivalent platinum drug not only can directly damage DNA and promote cell apoptosis, but also can induce ICD and activate T cells; the LOXL2 inhibitor further promotes immune infiltration of tumor tissues by degrading collagenous fibers and softening rigid ECM (extracellular matrix) of tumors, and the LOXL2 inhibitor and the LOXL2 inhibitor cooperatively kill tumor cells.
Owner:CHONGQING JIANGJIN DISTRICT CENT HOSPITAL

DNA double-strand break-capturing nuclear envelope tubules drive DNA repair

PCT designated stageWO2025137772A9Antibody ingredientsAmide active ingredientsNuclear membraneMedicine
The present disclosure describes a method of treating a dsbNETs-associated pathology or con- dition in a subject in need thereof, comprising administering a therapeutically effective amount of a dsbNETs modulator in the subject, wherein dsbNETs repair or misrepair damaged DNA or wherein excessively induced or persistent dsbNETs trigger DNA damage.
Owner:THE GOVERNING COUNCIL OF THE UNIV OF TORONTO

Gene expression regulation optimization technology based on target DNA recognition ultra-small molecular module

PCT designated stageWO2025254264A1HydrolasesAnimals/human peptidesGenome editingDna recognition
The present invention relates to a gene expression regulation optimization technology based on a target DNA recognition ultra-small molecular module, and relates to an ultra-small eCWCas12f-VPR system optimized through engineering of a CRISPR-Cas module, linking of activation domains, and various combinations of linkers and NLS sequences. It has been identified that effective and target-specific gene expression regulation superior to that of a conventional CRISPRa system can be achieved and the accuracy of the gene expression regulation is remarkably excellent. In particular, unlike a conventional CRISPR gene scissors technology, the system of the present invention can accurately regulate the expression of a target gene without cutting or damaging DNA, and thus is relatively safe and optimized for application in a gene therapy method, thereby exerting a great impact, and, due to the characteristics of ultra-small size, enables all genes to be loaded in a single vector (all-in-one), and thus can be effectively used as an excellent novel gene editing technology that compensates for the disadvantages of a conventional gene editing technology.
Owner:CHUNG ANG UNIV IND ACADEMIC COOP FOUND

An electrochemical method for detecting DNA damage based on CRISPR-Cas12a system

The application discloses an electrochemical method for detecting DNA damage based on a CRISPR-Cas12a system. Normal DNA can activate the activity of the CRISPR-Cas12a complex, resulting in the cutting of the DNA probe fixed on the electrode surface. The cut DNA probe cannot undergo HCR reaction in the presence of hairpin DNA H1 and H2, thereby generating a smaller electrochemical signal of methylene blue; damaged DNA cannot completely activate the activity of the CRISPR-Cas12a complex, at this time, the uncut DNA probe induces HCR in the presence of hairpin DNA H1 and H2 and generates longer double-stranded DNA, a large number of methylene blue molecules are combined with the double-stranded DNA, thereby generating a stronger electrochemical signal. The damage degree of DNA corresponds to the light damage level thereof, the electrochemical signal of methylene blue and the light damage level of DNA are in a linear relationship in the range of 0.021-0.42 kJ m ‑2 , and the lowest detection limit is 0.0088 kJ m ‑2 .
Owner:CENT SOUTH UNIV