1. Immunology/Inflammation
  2. PD-1/PD-L1
  3. SCL-1

SCL-1 is an orally active anti-PD-1/PD-L1 inhibitor. SCL-1 can inhibit PD-1/PD-L1 binding. SCL-1 increases T cells, B cells and natural killer cells. SCL-1 exerts strong tumor growth inhibitory effects that were mediated by effector T-cell induction inside tumors and the up-regulated expression of long non-coding RNAs as neoantigens leading to cytotoxic T lymphocyte activation. SCL-1 can be used for the research of cancer, such as triple-negative breast cancer.

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SCL-1

SCL-1 Chemical Structure

CAS No. : 1061105-16-5

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Description

SCL-1 is an orally active anti-PD-1/PD-L1 inhibitor. SCL-1 can inhibit PD-1/PD-L1 binding. SCL-1 increases T cells, B cells and natural killer cells. SCL-1 exerts strong tumor growth inhibitory effects that were mediated by effector T-cell induction inside tumors and the up-regulated expression of long non-coding RNAs as neoantigens leading to cytotoxic T lymphocyte activation. SCL-1 can be used for the research of cancer, such as triple-negative breast cancer[1][2].

In Vitro

SCL-1 (0.25-100 μM, 4 days) has no significant cytotoxicity in MDA-MB231 cell[1].
SCL-1 (25 μM) inhibits exhibits moderate inhibitory activities against PD-1/PD-L1 binding with inhibition rate of 63%[2].
SCL-1 inhibits SCC3 and Jurkat cell proliferation with IC50 values >50 μM[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

SCL-1 (25-100 mg/kg, p.o., 10 times over 14 days) inhibits tumor growth in humanized MDA-MB231 tumor tumor-bearing MHC-dKO NOG mice[1].
SCL-1 (50 mg/kg, p.o., 10 times over 14 days) suppresses tumor growth in humanized SCC-3 tumor-bearing MHC-dKO NOG mice[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: MDA-MB231 tumor in a humanized MHC-double knockout NOG mice models[1]
Dosage: 25, 50 and 100 mg/kg
Administration: Orally administered, 10 times over 14 days (days 1-5 and 8-12)
Result: Inhibited tumor volume.
Did not induce weight loss.
Increased infiltrated CD4+ and CD8+ T-cell numbers inside tumors.
Increased the frequency of CD19+ B cells that infiltrated tumors.
Showed high level of lymphoid cell infiltration.
Upregulated T cell-associated cytotoxic genes (GZMB, PRF1, and IFNB1), exhausted marker genes (PD-1, TIM3, and CD39), NK activation-associated genes (CD16 and NCR1), and T-cell attracting chemokine genes (CCL3 and CCL4).
Downregulated CXCL12 gene expression.
Upregulated tumor-specific long non-coding (lnc) RNAs.
Animal Model: Humanized SCC-3 tumor-bearing MHC-dKO NOG mice[2]
Dosage: 50 mg/kg
Administration: Orally administered, 10 times over 14 days (days 1-5 and 8-12)
Result: Promoted the engraftment of transplanted human PBMCs in the spleens.
Increased the number of infiltrated CD45+ human PBMCs and CD4+ and CD8+ T cells inside the tumors.
Had more foci of lymphoid cell infiltration with necrotic changes.
Increased CD8+ T cells.
Upregulated the expression of CXCL9 and CXCR3.
Downregulated the expression levels of CCL22 and TIM3.
Molecular Weight

396.41

Formula

C18H23F3N6O

CAS No.
SMILES

CC1CCCCN1C(C2CCN(CC2)C3=NN4C(C=C3)=NN=C4C(F)(F)F)=O

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    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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SCL-1
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HY-175604
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