SC-10 is a direct activator of protein kinase C (PKC) [1].
SC-10 targets protein kinase C (PKC), a family of serine/threonine kinases that play a central role in various signal transduction pathways. By acting as a direct activator, it induces histone phosphorylation by recombinant human PKC in a cell-free assay when used at concentrations ranging from 100 to 500 µM. This activation modulates downstream signaling pathways involved in cell proliferation, differentiation, and apoptosis.

When it comes to naive primary cells, SC-10 shows modulated biological effects, but it is unable to increase these cells' phosphoreceptives to cytotoxic medicines [1]. Ara-C-induced phosphoric acid reaction is inhibited by SC-10 [1].

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In U937 cells, SC-10 (10 μM, 72 h) caused a slight but statistically significant reduction in the percentage of cells in the G2/M cell cycle phase compared to untreated control cells. No significant changes in G1 or S phases were observed [1].
In HL-60 cells, SC-10 (10 μM, 72 h) did not significantly alter cell cycle distribution [1].
SC-10 (10 μM, 72 h) did not induce expression of p21WAF/CIP1, c-Fos, or c-Jun proteins in U937 cells as determined by Western blotting, whereas TPA (5 nM) strongly upregulated these proteins [1].
SC-10 (10 μM, 72 h) failed to cause membrane translocation of PKCα, PKCδ, or PKCε in U937 cells. Cytosolic and membrane fractions showed no alteration in PKC isoform content compared to untreated cells, whereas TPA induced clear translocation of all three isoforms [1].
SC-10 (10 μM, 72 h) did not down‑regulate the CD4 surface marker nor up‑regulate the β2‑integrin CD11c in U937 cells, indicating a lack of monocytic differentiation. In contrast, TPA strongly reduced CD4 and increased CD11c expression [1].
In U937 cells, pretreatment with SC-10 (10 μM, 1 h) followed by VP-16 (68 μM, 4 h) or Ara-C (1 μM, 24 h) did not significantly modulate the percentage of apoptotic (sub‑G1) cells compared to cytotoxic drug alone. TPA pretreatment significantly reduced apoptosis in both cases [1].
In HL-60 cells, pretreatment with SC-10 (10 μM, 1 h) followed by VP-16 (68 μM, 4 h) resulted in a minor but statistically significant reduction in apoptosis compared to VP-16 alone. TPA pretreatment enhanced apoptosis [1].
In HL-60 cells, pretreatment with SC-10 (10 μM, 1 h) followed by Ara-C (1 μM, 24 h) significantly inhibited Ara-C‑induced apoptosis (reached statistical significance). TPA pretreatment enhanced apoptosis [1].
In vitro, SC-10 is a direct activator of protein kinase C (PKC). It induces histone phosphorylation by recombinant human PKC in a cell-free assay at concentrations of 100-500 µM. It exhibits modest biological effects on leukemic blast cells but is not capable of enhancing the apoptotic response of these cells to cytotoxic drugs. It also inhibits the apoptotic response caused by Ara-C.

In vivo, SC-10 has been studied for its potential antiproliferative activity in leukemia research. As a PKC activator, it could modulate cell signaling pathways involved in cancer. However, specific in vivo efficacy data are not extensively detailed in the available literature.

In vitro kinase assays for SC-10 typically involve using purified recombinant human PKC. The enzyme is incubated with a substrate, such as histone, and ATP in the presence of varying concentrations of SC-10. The degree of substrate phosphorylation is then measured to assess the compound's ability to activate PKC.

Cell cycle analysis: Untreated or treated U937 and HL-60 cells (1×10⁶) were fixed with 70% ice‑cold ethanol overnight. Adherent cells were removed with a rubber policeman. After two washes with ice‑cold PBS, fixed cells were resuspended in 1 mL PBS containing propidium iodide (40 μg/mL) and RNase A (500 U/mL), incubated for 30 min in the dark, and analyzed by flow cytometry. Apoptotic populations were gated as objects with fluorescence values below 20% of the G1 peak. Propidium iodide fluorescence signal peak vs. integral was used to discriminate G2/M cells from G0/G1 doublets [1].
Cell surface marker analysis: 1×10⁶ cells were washed with PBS and resuspended in 1 mL PBS with 2% FCS. Aliquots (100 μL) were incubated at 4 °C with R‑phycoerythrin (PE)‑conjugated anti‑CD11c or PE‑conjugated anti‑CD4 for 10 min in the dark. After centrifugation, cells were resuspended in 500 μL PBS with 2% FCS and analyzed by flow cytometry [1].
Western blotting (immunoblot): Untreated or stimulated U937 cells were washed 3× in ice‑cold PBS and lysed in buffer containing 25 mM Tris–HCl (pH 7.6), 1 mM Na₃VO₄, 10 mM NaF, 10 mM EDTA, 10 μg/mL aprotinin, 10 μg/mL leupeptin, and 1 mM PMSF. Cells were swollen on ice for 30 min, homogenized with 30 strokes, and 1% NP‑40 was added. Homogenates were centrifuged at 15,000 g for 15 min at 4 °C. Protein concentration was adjusted by colorimetric assay. Equal loading was confirmed with anti‑β‑actin. Proteins were separated by SDS‑PAGE, transferred to PVDF membrane in transfer buffer (25 mM Tris–HCl, 192 mM glycine, 0.037% SDS, 20% methanol). Membranes were blocked with PBS containing 5% dried milk and 0.05% Tween‑20, washed, and incubated with primary antibodies against p21, c‑Fos, c‑Jun, PKCα, PKCδ, PKCε, or β‑actin. Bound antibodies were detected with peroxidase‑conjugated secondary antibodies (1:2000) for 1 h at room temperature and visualized by ECL autoradiography [1].
Subcellular fractionation for PKC translocation: After treatment, cells were lysed and separated into cytosolic and membrane fractions (method not detailed in this paper, but referenced as previous work). The protein fractions were subjected to Western blotting with anti‑PKCα, anti‑PKCδ, and anti‑PKCε antibodies [1].
Apoptosis quantification: After drug treatments, cells were fixed, stained with propidium iodide as described in cell cycle analysis, and the percentage of cells with sub‑G1 (hypodiploid) DNA content was measured by flow cytometry as a marker of late apoptosis/necrosis [1].
Dose‑response toxicity test: U937 cells were incubated with increasing concentrations of SC-10 (0, 1, 10, 50, 100 μM) for 72 h. Cells were ethanol‑fixed, stained with propidium iodide, and the sub‑G1 peak was quantified by flow cytometry to determine the percentage of dead cells. At 100 μM, SC-10 caused >85% cell death; 10 μM was used as a non‑toxic concentration for subsequent experiments [1].
In vitro cell-based assays for SC-10 have been performed on leukemic blast cells. Cells are treated with the compound, and the effects on cell viability (e.g., by MTT assay) and apoptosis (e.g., by measuring caspase activity) are assessed. Its effect on the apoptotic response to cytotoxic drugs like Ara-C can also be studied.

In vivo animal studies for SC-10 are not extensively detailed in the available literature. Potential studies could involve using mouse xenograft models of leukemia to assess its anti-tumor activity alone or in combination with other chemotherapeutic agents.

Specific pharmacokinetic properties of SC-10, such as half-life and bioavailability, are not detailed in the available literature. It is a research compound, typically used in vitro. It is soluble in DMSO and is supplied with a purity of ≥98%.

In vitro toxicity: In U937 cells, SC-10 at 100 μM for 72 h resulted in more than 85% cell death as measured by sub‑G1 DNA content (late apoptosis/necrosis). At 10 μM, no significant toxicity was observed [1]. No in vivo toxicity data were reported.
Comprehensive toxicological data for SC-10 are not provided in the available text. As a research compound, it is intended for laboratory use only and is not for human therapeutic use. Safety precautions should be followed when handling this compound.

[1]. Effect of novel modulators of protein kinase C activity upon chemotherapy-induced differentiation and apoptosis in myeloid leukemic cells. Anticancer Drugs. 2002 Aug;13(7):725-33.

5-Chloro-N-heptyl-1-naphthalenesulfonamide is a naphthalene compound and also a sulfonic acid derivative.

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SC-10 is a direct activator of protein kinase C (PKC) and is classified as a naphthalenesulfonamide PKC activator. Unlike phorbol esters such as TPA, SC-10 did not induce membrane translocation of PKCα, PKCδ, or PKCε in U937 cells, nor did it upregulate p21, c‑Fos, c‑Jun, or differentiation markers CD11c/CD4, suggesting that its biological effects are distinct from those of TPA. SC-10 exhibited only marginal effects on cell cycle distribution and showed a protective (anti‑apoptotic) effect against Ara‑C‑induced apoptosis in HL-60 cells, in contrast to the pro‑apoptotic effect of TPA. The compound failed to enhance the apoptotic response of leukemic cells to cytotoxic drugs VP‑16 and Ara‑C in U937 cells [1].
SC-10 is a direct activator of protein kinase C (PKC). It is a valuable tool for studying the role of PKC in cell signaling and for investigating potential therapeutic strategies in leukemia. It is also known as N-(6-phenylhexyl)-5-chloro-1-naphthalenesulfonamide. This product is for research use only.

339.106

C, 60.08; H, 6.52; Cl, 10.43; N, 4.12; O, 9.41; S, 9.43

102649-79-6

102649-79-6;

5175

White to off-white solid powder

1.192g/cm3

483.2ºC at 760 mmHg

246ºC

1.72E-09mmHg at 25°C

1.573

6.213

1

3

8

22

421

0

MJMJERJFCHYXEM-UHFFFAOYSA-N

InChI=1S/C17H22ClNO2S/c1-2-3-4-5-6-13-19-22(20,21)17-12-8-9-14-15(17)10-7-11-16(14)18/h7-12,19H,2-6,13H2,1H3

5-chloro-N-heptylnaphthalene-1-sulfonamide

SC-10 SC10 SC 10

2934.99.03.00

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)