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Results for "

ROR1

" in MedChemExpress (MCE) Product Catalog:

11

Inhibitors & Agonists

1

Peptides

2

Inhibitory Antibodies

7

Recombinant Proteins

1

Antibodies

1

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P99201
    Zilovertamab
    1 Publications Verification

    UC-961; Cirmtuzumab

    		 ROR Cancer
    Zilovertamab (UC-961) is a humanised monoclonal antibody against ROR1 that blocks Wnt5a-induced ROR1 signalling [1].
    Zilovertamab
  • HY-139534
    ARI-1

    		ROR Apoptosis Cancer
    ARI-1 is an inhibitor of receptor tyrosine kinase-like orphan receptor 1 (ROR1) inhibitor. ARI-1 effectively inhibits aberrant ROR1 expression, which is associated with the development of non-small cell lung cancer (NSCLC) and EGFR-TKI-induced drug resistance. ARI-1 binds to the extracellular Frizzled domain of ROR1 and regulates PI3K/AKT/mTOR signaling in a ROR1-dependent manner. ARI-1 potently inhibits NSCLC cell proliferation and migration and has antitumor activity in vivo [1] .
    ARI-1
  • HY-139534A
    (S)-ARI-1

    		Drug Isomer Others
    (S)-ARI-1 is an S-enantiomer of ARI-1. ARI-1 is a ROR1 inhibitor and apoptosis inducer, used in NSCLC research [1].
    (S)-ARI-1
  • HY-161096
    Antitumor agent-127

    		ROR Cancer
    Antitumor agent-127 (compound 1) is a parent macrocyclic peptide. Antitumor agent-127 displays nanomolar cell-based binding to ROR1 and relatively good internalization in 786-O and MDA-MB-231 tumor cell lines [1].
    Antitumor agent-127
  • HY-P99956
    Zilovertamab vedotin

    VLS-101; MK-2140

    		 Antibody-Drug Conjugates (ADCs) Apoptosis Cancer
    Zilovertamab vedotin (VLS-101) is a novel antibody-drug conjugate comprising the humanized monoclonal antibody zilovertamab and and the anti-microtubule cytotoxin monomethyl vedotin. Zilovertamab vedotin binding to tumor cell ROR1 results in rapid internalization, trafficking to lysosomes, antibody–agent conjugate cleavage, and monomethyl vedotin release. Zilovertamab vedotin induces apoptosis. Zilovertamab vedotin can be used in research of cancer [1].
    Zilovertamab vedotin
  • HY-170996
    ROR1 ligand-1

    		ROR Cancer
    ROR1 ligand-1 (9-1) is a ligand for PROTACT ROR1 degrader-1 (HY-170995). ROR1 ligand-1 connects with VHL-type or CRBN ligand to design and synthesize the first selective and potent of ROR1 PROTACs [1].
    ROR1 ligand-1
  • HY-RS12124
    ROR1 Human Pre-designed siRNA Set A

    		Small Interfering RNA (siRNA) Others

    ROR1 Human Pre-designed siRNA Set A contains three designed siRNAs for ROR1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.

    ROR1 Human Pre-designed siRNA Set A
    ROR1 Human Pre-designed siRNA Set A
  • HY-162640
    ROR1-IN-1

    		ROR Cancer
    ROR1-IN-1 (Compound 19h) is an inhibitor for receptor tyrosine kinase-like orphan receptor 1 (ROR 1) with Ki of 0.10 μM. ROR1-IN-1 inhibits proliferation of cancer cells H1975, A549 and MDA-MB-231, with IC50 of 0.36 μM, 1.37 μM and 0.47 μM. ROR1-IN-1 exhibits antitumor efficacy in mice and good pharmacokinetic characteristics in rat models [1].
    ROR1-IN-1
  • HY-170995
    PROTAC ROR1 degrader-1

    		ROR Apoptosis Cancer
    PROTAC ROR1 degrader-1 (Compound 11d) is a PROTAC degrader for pseudokinase ROR1 that degrades ROR1 in NSCLC cells with a DC50s of 40-80 nM. PROTAC ROR1 degrader-1 causes the cleavage of PARP and induces apoptosis in NCI-H23 [1]. (Pink: ligand for target protein ROR1 ligand-1 (HY-170996); Black: linker (HY-W014787); Blue: ligand for VHL E3 ligase (S,R,S)-AHPC (HY-125845))
    PROTAC ROR1 degrader-1
  • HY-160790
    β-Glu-PNP

    		ADC Linker Cancer
    β-Glu-PNP is an ADC linker used in the synthesis of antibody-drug conjugates (ADCs) [1].
    β-Glu-PNP
  • HY-117947
    (R)-OR-S1

    		Histone Methyltransferase Cancer
    (R)-OR-S1 is an isomer of OR-S1. The dual ZH1/2 inhibitors OR-S1 and OR-S2 exhibit strong inhibitory activity against both EZH1 and EZH2. OR-S1 and OR-S2 are highly selective methyltransferase inhibitors against EZH1 and EZH2, and they have very similar molecular features. Therefore, we investigated the effect of OR-S1 on acute myeloid leukemia (AML). We found that OR-S1 was able to induce cell differentiation and apoptosis in AML cells. These findings encouraged us to investigate whether functional LT-HSCs could survive PRC2-targeted therapy with OR-S1 or OR-S1 combined with cytarabine. The results showed that OR-S1 did not cause significant myelosuppression, and BM cells treated with the combination therapy were able to undergo normal hematopoiesis even 4 months after treatment. Therefore, temporary inhibition of EZH1 and EZH2 is clinically tolerable, making this combination therapy suitable for AML patients. AML is generally believed to originate from myeloid progenitor cells that inherit a large number of biological properties.
    (R)-OR-S1

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