C021 dihydrochloride c021

Manufactured by Bio-Techne

Sourced in United Kingdom, United States

C021 dihydrochloride (C021) is a reagent used in laboratory settings. It serves as a core component in various research applications. The detailed functionality and intended use of this product should be obtained from official product documentation or technical support.

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Lab products found in correlation

3 protocols using c021 dihydrochloride c021

Intrathecal Opioid and Chemokine Modulation

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C021 dihydrochloride (C021; CCR4 antagonist; Tocris, Bristol, UK); morphine hydrochloride [M; μ-opioid receptor (MOR), δ-opioid receptor (DOR), and κ-opioid receptor (KOR) agonist; TEVA, Kutno, Poland]; buprenorphine [B; MOR and nociceptin receptor (NOR) agonist and DOR and KOR antagonist; Polfa S.A., Warsaw, Poland], and recombinant mouse CCL17/CCL22/CCL2 proteins (R&D Systems, Minneapolis, USA) were dissolved in water for injection. The control groups received water for injection (V) on the same schedule. The substances were administered i.t. or i.p. The i.t. injections were performed using a Hamilton syringe with a thin needle in accordance with the literature (30 (link)). The substances were injected into the lumbar part of the spinal cord (between the L5 and L6 vertebral space) in a volume of 5 μl. The i.p. injections were performed in accordance with PolLASA (Polish Laboratory Animal Science Association) guidelines.

Bogacka J., Ciapała K., Pawlik K., Kwiatkowski K., Dobrogowski J., Przeklasa-Muszynska A, & Mika J. (2020). CCR4 Antagonist (C021) Administration Diminishes Hypersensitivity and Enhances the Analgesic Potency of Morphine and Buprenorphine in a Mouse Model of Neuropathic Pain. Frontiers in Immunology, 11, 1241.

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Antineoplastic Agents and Liposomal Formulations

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Reagents and solvents were purchased from Sigma-Aldrich (St. Louis, MO) and used without further purification, unless otherwise indicated. Water was purified by MilliQ filtration systems (Millipore) prior to experimental use. Trametinib (Tram), gemcitabine (Gem), and paclitaxel (PTX) were purchased from LC Laboratories (Woburn, MA). STEALTH liposomal doxorubicin HCl (Doxil) and DiI-labelled PEGylated DOPC/CHOL liposomes (Lip) were purchased from FormuMax (Sunnyvale, CA). Pharmacy-grade nanoparticulate albumin-bound paclitaxel (nab-PTX, trade name: Abraxane®; Celgene; Summit, NJ) was purchased form McKesson (Irving, Taxes). CFI400945 fumarate (CFI400945), AXL1717^{46 (link)}, VX-745, AZD-7762, JNK-IN-8, AZD-1390, Bindarit, MK-8033, AS602801, cobimetinib, refametinib, MK-8353, SCH772984, A-769662, Compound C dihydrochloride (Compound C), and Linsitinib (Lin)^{47 (link)} were all purchased from MedChemExpress (Monmouth Junction, NJ). RepSox, 7rh, Y-27632 dihydrochloride (Y-27632), and C 021 dihydrochloride (C021) were purchased from Tocris (Bristol, UK), Sigma, Abcam (Cambridge, MA), and R&D Systems (Minneapolis, MN), respectively. 5-(N-Ethyl-N-isopropyl)amiloride (EIPA) was purchased from Sigma-Aldrich.

Li R., Ng T.S., Wang S.J., Prytyskach M., Rodell C.B., Mikula H., Kohler R.H., Garlin M.A., Lauffenburger D.A., Parangi S., Dinulescu D.M., Bardeesy N., Weissleder R, & Miller M.A. (2021). Therapeutically reprogrammed nutrient signaling enhances nanoparticulate albumin bound drug uptake and efficacy in KRAS-mutant cancer. Nature nanotechnology, 16(7), 830-839.

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Antibody and Chemical Reagent Sources

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Antibodies against IBA1 were purchased from Wako Chemicals USA (Richmond, VA, USA). Antibodies against CCL2, CCR2, and CCR4 were purchased from Genetex (Irvine, CA, USA). NeuN antibodies were ordered from Millipore (Billerica, MA, USA). All real-time PCR (RT-PCR) primers were purchased from SABiosciences (Frederick, MD, USA). INCB 3284 dimesylate (INCB) and C021 dihydrochloride (C021) were purchased from Tocris Bioscience (Minneapolis, MN, USA). All other chemicals were purchased from Sigma-Aldrich (St. Louis, MO, USA) unless otherwise noted, and were of the highest grade available.

McMillin M., Frampton G., Thompson M., Galindo C., Standeford H., Whittington E., Alpini G, & DeMorrow S. (2014). Neuronal CCL2 is upregulated during hepatic encephalopathy and contributes to microglia activation and neurological decline. Journal of Neuroinflammation, 11, 121.

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