| Size | Price | Stock | Qty |
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| 1mg |
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| 5mg | |||
| 10mg | |||
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| Targets |
CD47/SIRPα axis[1]
CD47 (Cluster of Differentiation 47) and SIRPalpha (Signal Regulatory Protein Alpha). This compound inhibits the binding of CD47, often overexpressed on cancer cells, to its receptor SIRPalpha on macrophages, thereby blocking the inhibitory signal that prevents phagocytosis. |
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| ln Vitro |
In vitro, NCGC00138783 TFA promotes macrophage-mediated phagocytosis of cancer cells by blocking the CD47-SIRPalpha interaction. It enhances the engulfment of tumor cells by bone marrow-derived macrophages (BMDMs) in co-culture assays, demonstrating its potential to activate the innate immune system against cancer cells at an IC50 of 50 microM.
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| ln Vivo |
In vivo efficacy studies for this CD47 inhibitor are typically conducted using syngeneic mouse tumor models, such as the B16-F10 melanoma or CT26 colon carcinoma model. Mice are treated intravenously or intratumorally with NCGC00138783 TFA, and tumor growth inhibition (TGI) is monitored. Enhanced infiltration of phagocytic cells (e.g., macrophages) into the tumor is typically observed.
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| Enzyme Assay |
A biochemical non-cellular binding assay to evaluate CD47-SIRPalpha interaction is performed using surface plasmon resonance (SPR) or ELISA. For SPR, recombinant CD47 protein is immobilized on a sensor chip, and varying concentrations of the test compound (NCGC00138783) are injected with a fixed concentration of SIRPalpha. The change in response units (RU) is measured to determine the inhibition of binding. ELISA would use a plate coated with CD47 and a labeled SIRPalpha.
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| Cell Assay |
In vitro cellular assays to assess CD47 blockade involve a phagocytosis assay. In this set-up, cancer cell lines (e.g., Jurkat T cells or Raji B cells) are labeled with a fluorescent dye (e.g., CFSE). These target cells are co-incubated with primary human or mouse macrophages (effector cells) in the presence of serial dilutions of NCGC00138783 TFA. After 1-2 hours, phagocytosis is quantified by flow cytometry as the percentage of macrophages that are also fluorescent-positive (e.g., F4/80+/CFSE+).
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| Animal Protocol |
In vivo animal studies using a syngeneic mouse tumor model are conducted as follows: Female C57BL/6 mice are injected subcutaneously with B16-F10 tumor cells. When tumors reach a size of ~100 mm3, mice are randomized into treatment groups. NCGC00138783 TFA is administered (e.g., 10 mg/kg, i.p., daily). Tumor volumes are measured with calipers every 2-3 days. At the study endpoint, tumors are excised and analyzed for immune cell infiltration (e.g., macrophages, CD8+ T cells) by IHC or flow cytometry.
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| ADME/Pharmacokinetics |
Preclinical pharmacokinetic data (e.g., half-life, clearance, oral bioavailability) for this specific CD47 inhibitor are not widely available in standard public databases. As a research tool compound, its use in vivo has been limited, and its absorption, distribution, metabolism, and excretion (ADME) properties have not been fully characterized.
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| Toxicity/Toxicokinetics |
Detailed pre-clinical toxicology profiles (e.g., LD50, NOAEL) for NCGC00138783 TFA are not available in standard public databases. As an inhibitor of the CD47-SIRPalpha pathway, potential on-target toxicities could include anemia or thrombocytopenia due to increased phagocytosis of red blood cells or platelets, which also express CD47.
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| References |
[1]. Junqiao Zhu, et al. CD47-SIRPα axis in cancer therapy: Precise delivery of CD47-targeted therapeutics and design of anti-phagocytic drug delivery systems. Medicine in Drug Discovery. 2022. 15:100139
[2]. Bo Huang, et al. Structural analysis and binding sites of inhibitors targeting the CD47/SIRPα interaction in anticancer therapy. Comput Struct Biotechnol J. 2021 Oct 1;19:5494-5503. |
| Additional Infomation |
The CD47/SIRPalpha axis is a well-validated "don't eat me" checkpoint in immunotherapy, and its blockade is being actively pursued as a cancer treatment. NCGC00138783 TFA serves as a tool compound for academic research to study the biology of this pathway. It has not been approved for clinical use.
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| Molecular Formula |
C28H27F4N7O3S
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| Related CAS # |
NCGC00138783;NCGC00138783 free base;896700-07-5
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| Appearance |
White to light yellow solid powder
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment (e.g. under nitrogen), avoid exposure to moisture and light. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO :~50 mg/mL (~80.96 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 1.25 mg/mL (2.02 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 12.5 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. (Please use freshly prepared in vivo formulations for optimal results.) |
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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