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dMCL1-2 - CAS 2351218-88-5

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dMCL1-2 is a potent and selective degrader of myeloid cell leukemia 1 (MCL1) based on PROTAC, which binds to MCL1 with a KD of 30 nM. dMCL1-2 activats the cellular apoptosis machinery by degradation of MCL1.

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Molecular Formula

C61H66N10O12S

Molecular Weight

1163.3

dMCL1-2

- Specification
  - Solubility
    
    10 mM in DMSO
    
    Storage
    
    Please store the product under the recommended conditions in the Certificate of Analysis.
    
    Shipping
    
    Room temperature in continental US; may vary elsewhere
    
    Synonyms
    
    dMCL1-2; dMCL1 2; dMCL12; 7-[5-[[4-[4-(dimethylsulfamoyl)piperazin-1-yl]phenoxy]methyl]-1,3-dimethylpyrazol-4-yl]-1-[2-[4-[2-[2-(2,6-dioxopiperidin-3-yl)-1,3-dioxoisoindol-4-yl]oxyacetyl]piperazin-1-yl]ethyl]-3-(3-naphthalen-1-yloxypropyl)indole-2-carboxylic acid
- Properties
  - InChI Key
    
    VPWUIQNEJHXPSK-UHFFFAOYSA-N
    
    InChI
    
    InChI=1S/C61H66N10O12S/c1-39-54(49(65(4)63-39)37-82-42-22-20-41(21-23-42)67-31-33-69(34-32-67)84(79,80)64(2)3)46-15-8-14-44-45(17-10-36-81-50-18-7-12-40-11-5-6-13-43(40)50)57(61(77)78)70(56(44)46)35-28-66-26-29-68(30-27-66)53(73)38-83-51-19-9-16-47-55(51)60(76)71(59(47)75)48-24-25-52(72)62-58(48)74/h5-9,11-16,18-23,48H,10,17,24-38H2,1-4H3,(H,77,78)(H,62,72,74)
    
    Canonical SMILES
    
    CC1=NN(C(=C1C2=CC=CC3=C2N(C(=C3CCCOC4=CC=CC5=CC=CC=C54)C(=O)O)CCN6CCN(CC6)C(=O)COC7=CC=CC8=C7C(=O)N(C8=O)C9CCC(=O)NC9=O)COC1=CC=C(C=C1)N1CCN(CC1)S(=O)(=O)N(C)C)C
- Reference Reading
  - 1. ADAM protease inhibition overcomes resistance of breast cancer stem-like cells to γδ T cell immunotherapy
    
    Indrani Dutta, Dylan Dieters-Castator, James W Papatzimas, Anais Medina, Julia Schueler, Darren J Derksen, Gilles Lajoie, Lynne-Marie Postovit, Gabrielle M Siegers Cancer Lett. 2021 Jan 1;496:156-168. doi: 10.1016/j.canlet.2020.10.013.Epub 2020 Oct 10.
    
    Gamma delta T cells (γδTc) have tremendous anti-tumoral activity, thus γδTc immunotherapy is currently under development for various malignancies. We targeted breast cancer stem-like cells (BCSC), a rare cell population responsible for patient mortality. BCSC were mostly susceptible to γδTc immunotherapy, yet some escaped. The BCSC secretome rendered γδTc hypo-responsive, and resistant BCSC expressed more PD-L1 and anti-apoptotic protein MCL-1 than non-stem-like cells (NSC). BCSC resistance was partially overcome by dMCL1-2, an MCL-1 degrader, or more fully by blocking PD-1 on γδTc. Increased MICA shedding was prevented by the ADAM inhibitor GW280264X, rendering BCSC as sensitive to γδTc cytotoxicity as NSC. Our data show promising potential for γδTc immunotherapy against BCSC while unraveling immune evasion mechanisms exploited by BCSC, which likely also enable their resistance to cytotoxic T and NK cells. Overcoming this resistance, as we have done here, will improve cancer immunotherapy, leading to better cancer patient outcomes.

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