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Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!2025-02-06
188 Results for "
regression
" in MedChemExpress (MCE) Product Catalog:
Products (188)
188 Results for "regression" in MCE Product Catalog:
Cat. No.: HY-164429
CAS No.: 2418533-90-9
VIP236 is a small-molecule drug conjugate targeting αvβ3 integrin. VIP236 achieves tumor homing via specific binding to αvβ3 integrin and delivers its payload to the tumor microenvironment. The linker of VIP236 is cleavable by neutrophil elastase, which is highly expressed in the tumor microenvironment, to release the payload 7-ethylcamptothecin. This payload induces DNA damage by inhibiting topoisomerase 1, thereby exerting anti-tumor effects. VIP236 exhibits excellent plasma stability and tumor targeting property, with a tumor/plasma payload ratio 10-fold higher than that of the single administration. It effectively induces tumor regression, reduces metastasis formation, and shows good tolerance in mouse models. VIP236 has been used in studies related to non-small cell lung cancer, clear cell renal cell carcinoma, colon cancer, triple-negative breast cancer, small cell lung cancer, and metastatic solid tumors .
Cat. No.: HY-181420
CAS No.: 3029184-80-0
Target:
Research Areas:
(S,R,S)-BBO-11818 is an orally active, highly selective (relative to NRAS and HRAS), non-covalent pan-KRAS inhibitor (IC50=28-120 nM). (S,R,S)-BBO-11818 specifically binds to the Switch-II/Helix 3 pocket, disrupts the KRAS:RAF1 interaction by inducing conformational changes, and blocks the MAPK signaling pathway. (S,R,S)-BBO-11818 exhibits significant anti-tumor activity, which not only inhibits cell proliferation and induces apoptosis, but also drives tumor regression in xenograft models. (S,R,S)-BBO-11818 produces synergistic effects when combined with Cetuximab (HY-P9905), anti-PD-1 antibody or PI3Kα inhibitor. (S,R,S)-BBO-11818 is used in the research of KRAS mutation-related malignancies such as pancreatic cancer, non-small cell lung cancer and colorectal cancer .
Cat. No.: HY-188120
Research Areas:
AZD5335 is an ADC targeting FRα, with an IC50 of 10.6 nM against human FRα. AZD5335 specifically binds to FRα, mediates internalization and trafficking to lysosomal compartments, while delivering a topoisomerase I inhibitor payload that traps TOP1-DNA cleavage complexes. AZD5335 induces DNA damage response via the ATR, ATM, Chk1 and Chk2 signaling pathways, and increases the levels of phosphorylated KAP1, phosphorylated RPA, phosphorylated γH2AX, as well as PARP cleavage. AZD5335 exhibits bystander cytotoxicity against FRα-negative cells co-cultured with FRα-expressing cells. AZD5335 induces potent and durable responses and complete regression in ovarian cancer models, including models with low FRα expression and models resistant to Elahere, with enhanced efficacy when combined with Carboplatin, Bevacizumab or poly (ADP-ribose) polymerase inhibitors. AZD5335 can be used for ovarian cancer research .
Cat. No.: HY-163962
CAS No.: 2451070-32-7
Target:
PROTACs Btk Bcr-Abl Toll-like Receptor (TLR) Fc Receptor (FcR) NOD-like Receptor (NLR) PERK p38 MAPK NF-κB TNF Receptor
Research Areas:
L18I is a Bruton's tyrosine kinase (BTK) PROTAC degrader that targets wild-type and BTK C481, and recruits the cereblon E3 ligase to mediate proteasomal degradation. L18I regulates the BCR, TLR, FcγR and NLRP3 inflammasome signaling pathways, inhibits the phosphorylation of PLCγ-2, ERK1/2 and p38, and reduces the levels of B cell activation markers CD25, CD69 and CD86. L18I downregulates the NF-κB, TNF and TLR signaling pathways, reduces the production of pro-inflammatory cytokines, and decreases immune cell infiltration and immune complex deposition. L18I inhibits the proliferation of BTK-expressing lymphoma cells, induces tumor regression in xenograft models, and exhibits synergistic activity when combined with inhibitors of SYK, PI3K or Lyn. L18I can be used in research related to lupus, diffuse alveolar hemorrhage and B-cell lymphoma .
Cat. No.: HY-164919
CAS No.: 2847102-44-5
Synonyms: XMT-2056
Research Areas:
Calotatug ginistinag (XMT-2056) is an antibody-drug conjugate (ADC) targeting HER2, linked to a payload composed of XMT-1519 conjugate-1 (HY-148067) and STING agonist-20 (HY-148068). Calotatug ginistinag activates the STING signaling pathway in tumor cells and tumor-resident immune cells, induces the production of type I interferons and cytokines (CXCL10, IFN-β, IL-6, TNF-α, triggers innate anti-tumor immune responses, and exerts a bystander effect. Calotatug ginistinag exhibits efficacy against HER2-expressing cancer cells in co-culture with PBMCs. Calotatug ginistinag induces tumor regression and reduces systemic inflammation in various tumor models. Combination treatment with Calotatug ginistinag, Trastuzumab (HY-P9907) and T-DXd (HY-138298) yields benefits. Calotatug ginistinag can be used in studies related to HER2-expressing solid tumors such as breast cancer, gastric cancer and ovarian cancer .
Cat. No.: HY-178061
CAS No.: 2598870-24-5
APS03118 is an orally active, potent and selective rearranged during transfection (RET) inhibitor. APS03118 broadly inhibits RET fusions and mutations (including G810, V804, L730, and Y806 variants), with IC50 values predominantly below 1 nM (0.095 nM for WT; ranging from 0.00438 to 5.72 nM for mutants), and demonstrates marked superiority against RET G810 mutations. APS03118 inhibits the entire RET signaling pathway (including RET, Shc, and ERK1/2), with >20-fold selectivity over most off-target kinases (except FLT3 and YES). APS03118 induces complete tumor regression in KIF5B-RET and CCDC6-RET V804 M patient derived xenografts (PDXs) and significantly prolongs survival in an intracranial CCDC6-RET metastasis mice model. APS03118 can be used for selective RET inhibitor (SRI)-resistant, RET-driven cancer research .
Cat. No.: HY-132031
CAS No.: 2682939-53-1
Target:
Research Areas:
Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 is a drug-linker conjugate composed of a cleavable Val-Ala linker and the potent ADC cytotoxin PNU-159682 (HY-16700), which is applicable for ADC synthesis. When conjugated with an anti-CD46 antibody, Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 delivers its payload to CD46-expressing cells, while cathepsin B cleaves the Val-Ala linker to release the payload. ADCs synthesized from Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 drive durable responses in CD46-expressing patient-derived xenograft models of non-small cell lung cancer and colorectal cancer, and a single administration induces complete tumor regression in most models. Mal-Val-Ala-PAB (C2-glucuronic acid)-DMEA-PNU-159682 can be used in the research of non-small cell lung cancer and colorectal cancer .
Cat. No.: HY-P990688
CAS No.: 2559056-68-5
Synonyms: AMG-509
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Protocols
Targeted therapy! The Capetin Prize winning "Click Chemistry" can be used like this!Targeted therapy! The Nobel Prize winning "Click Chemistry" can be used like this!A suitable model is crucial in drug screening experiments. Organs can mimic the three-dimensional functional structure of internal organs, have similar spatial organization to corresponding organs, maintain some key characteristics, and reproduce some physiological functions. They are widely used for modeling and personalized drug screening physiological functions.2025-02-06
