2. Metabolic Enzyme/Protease Cell Cycle/DNA Damage Apoptosis Autophagy PI3K/Akt/mTOR Anti-infection
  3. Stearoyl-CoA Desaturase (SCD) DNA/RNA Synthesis Apoptosis Autophagy mTOR Influenza Virus
  4. SSI-4

SSI-4 is an orally active stearoyl-CoA desaturase (SCD1) inhibitor with an EC50 of 1.9 nM against mouse SCD1. SSI-4 blocks the conversion of saturated fatty acids to monounsaturated fatty acids, reducing the production of oleic acid and palmitoleic acid. SSI-4 induces lipid peroxidation, endoplasmic reticulum stress, DNA damage and activates apoptotic mechanisms. SSI-4 inhibits mTORC1 activity, suppresses B cell proliferation and antibody production, and induces autophagy. SSI-4 is applicable to research on cancers such as acute myeloid leukemia and renal cell carcinoma, as well as influenza infections.

For research use only. We do not sell to patients.

SSI-4

SSI-4 Chemical Structure

CAS No. : 1875084-68-6

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SSI-4 Related Antibodies

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Description

SSI-4 is an orally active stearoyl-CoA desaturase (SCD1) inhibitor with an EC50 of 1.9 nM against mouse SCD1. SSI-4 blocks the conversion of saturated fatty acids to monounsaturated fatty acids, reducing the production of oleic acid and palmitoleic acid. SSI-4 induces lipid peroxidation, endoplasmic reticulum stress, DNA damage and activates apoptotic mechanisms. SSI-4 inhibits mTORC1 activity, suppresses B cell proliferation and antibody production, and induces autophagy. SSI-4 is applicable to research on cancers such as acute myeloid leukemia and renal cell carcinoma, as well as influenza infections[1][2][3][4].

IC50 & Target

SCD1[1]
In Vitro

SSI-4 (1 μM; 21 d) inhibits the proliferation of human acute myeloid leukemia (AmL) cell lines MOLM-13, MV-4-11 and OCI-AmL3, with differential activity observed across these cell lines[1].
SSI-4 (0.01-10 μM; 72 h) induces dose-dependent cell death in sensitive human acute myeloid leukemia cell lines K562, MOLM-13, and MV-4-11, but exerts no such effect in resistant human acute myeloid leukemia cell lines OCI-AmL3, THP-1, HL-60, Kasumi-1, and TF-1[1].
SSI-4 (1-10 μM; 4-7 d) induces cell death in primary samples from a subset of human AmL patients, and its sensitivity is independent of specific driver mutations[1].
SSI-4 (1 μM; 24 h) inhibits de novo monounsaturated fatty acid (MUFA) biosynthesis and increases the accumulation of saturated fatty acid (SFA) in the sensitive human acute myeloid leukemia cell lines MOLM-13 and MV-4-11, but exerts minimal effects on fatty acid biosynthesis in the drug-resistant OCI-AmL3 cells[1].
SSI-4 (1 μM; 24 h) significantly increases the SFA/MUFA ratio in sensitive human acute myeloid leukemia cell lines K562, MOLM-13 and MV-4-11, but exerts no such effect on drug-resistant human acute myeloid leukemia cell lines OCI-AmL3, THP-1 and HL-60[1].
SSI-4 (1 μM; 24 h) induces lipid peroxidation in sensitive human acute myeloid leukemia (AmL) cell lines K562, MOLM-13 and MV-4-11, but exerts no such effect in drug-resistant human AmL cell lines OCI-AmL3, THP-1, HL-60 and Kasumi-1[1].
SSI-4 (1 μM; 72 h) induces early apoptosis in the human AmL cell line MOLM-13[1].
When used in combination with palmitic acid, SSI-4 (1 μM; 72 h) activates apoptotic mechanisms in both the sensitive human acute myeloid leukemia cell line MOLM-13 and the drug-resistant human acute myeloid leukemia cell line OCI-AmL3[1].
SSI-4 (1 μM; 72 h) induces apoptosis in the sensitive human acute myeloid leukemia (AmL) cell lines MOLM-13 and MV-4-11, and this effect is partially reversed by pan-caspase inhibition[1].
SSI-4 (1 μM; 24 h) induces mild DNA damage in the human AmL cell line MV-4-11 and enhances palmitic acid- or doxorubicin-induced DNA damage[1].
SSI-4 (0-1000 nM; 72 h) acts synergistically with doxorubicin to reduce the viability of the human acute myeloid leukemia cell line MV-4-11[1].
SSI-4 inhibits stearoyl-CoA desaturase-mediated monounsaturated fatty acid accumulation in LPS/IL-4 activated mouse B cells[2].
SSI-4 (48 h) blocks de novo glucose synthesis of monounsaturated fatty acids in activated mouse B cells[2].
SSI-4 (1 μM; 3 d) dose-dependently inhibits the proliferation of mouse B cells activated by LPS/IL-4 and reduces cell viability at 72 h, while exogenous oleic acid reverses these effects[2].
SSI-4 (3 d) inhibits the proliferation of mouse B cells activated by anti-IgM/anti-CD40/IL-4 or CpG/IL-4/IL-5, and this effect is reversible by exogenous oleic acid[2].
SSI-4 (3 d) inhibits IgG1 class switching in mouse B cells activated by LPS/IL-4, and this effect is reversed by exogenous oleic acid[2].
SSI-4 inhibits the proliferation of activated human B cells, and this effect can be reversed by exogenous oleic acid[2].
SSI-4 reduces the expression of CD80 and CD86 on activated human B cells, and this effect can be reversed by exogenous oleic acid[2].
SSI-4 impairs the metabolic adaptability of activated mouse B cells by simultaneously reducing the levels of oxidative phosphorylation and glycolysis[2].
SSI-4 induces excessive autophagosome formation in activated mouse B cells[2].
SSI-4 induces autophagy, inhibits mTORC1 activity (decreased p-S6 level), and downregulates AID expression in activated mouse B cells, while all these effects are reversed by exogenous oleic acid[2].
SSI-4 induces endoplasmic reticulum stress in activated mouse B cells, and this effect is reversed by exogenous oleic acid[2].
SSI-4 potently blocks the conversion of saturated fatty acids to monounsaturated fatty acids in mouse liver microsomes, with an EC50 of 1.9 nM[3].
SSI-4 (0.001-0.009 μM; 72 h) potently inhibits the proliferation of ccRCC cell lines A498, ACHN, Caki1 and Caki2, with IC50 values ranging from 0.001 to 0.009 μM[4].
SSI-4 (0.001-0.009 μM) upregulates BiP and CHOP, specific markers of the stearoyl-CoA desaturase 1 (SCD1)-dependent unfolded protein response, in A498 and ACHN cells, and this effect is reversed by oleic acid supplementation[4].
SSI-4 (10-100 nM) exhibits high kinome selectivity, with no off-target kinase binding at 10 nM, and only binds to CDKL2 at 100 nM[4].

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

SSI-4 Related Antibodies

Cell Proliferation Assay[1]

Cell Line: human acute myeloid leukemia AML cell lines MOLM-13, MV-4-11, OCI-AML3
Concentration: 1 μM
Incubation Time: 6 cycles of 72 h over 21 days total
Result: Reduced cumulative cell divisions in all three cell lines tested, with the strongest inhibition observed in MOLM-13 cells, followed by MV-4-11 cells, and the weakest inhibition in OCI-AML3 cells.

Apoptosis Analysis[1]

Cell Line: human AML cell line MOLM-13
Concentration: 1 μM
Incubation Time: 72 h
Result: Significantly increased early apoptosis in MOLM-13 cells.

Western Blot Analysis[1]

Cell Line: human AML cell lines MOLM-13, OCI-AML3
Concentration: 1 μM
Incubation Time: 72 h
Result: Induced cleavage of PARP and caspase 3 in both MOLM-13 and resistant OCI-AML3 cells grown in the presence of palmitate.

Apoptosis Analysis[1]

Cell Line: human AML cell lines MOLM-13, MV-4-11
Concentration: 1 μM
Incubation Time: 72 h
Result: Induced cell death in both MOLM-13 and MV-4-11 cells, with partial rescue observed when co-treated with pan-caspase inhibitor Q-VD-OPh, though the effect was not fully abrogated.
Parmacokinetics
Species Dose Route Cmax T1/2 AUC0-inf Bioavailability
Rat[4] 10 mg/kg p.o. 4323 ng/mL 3.48 h 20922 ng·h/mL 119 %
Rat[4] 30 mg/kg p.o. 15900 ng/mL 2.71 h 71229 ng·h/mL 152 %
Rat[4] 100 mg/kg p.o. 43267 ng/mL 3.94 h 336456 ng·h/mL 212 %
In Vivo

SSI-4 (10 mg/kg; p.o.; daily administration; for 9 consecutive days) significantly extends the survival of NBSGW mice bearing MV-4-11 acute myeloid leukemia xenografts[1].
SSI-4 (10 mg/kg; p.o.; once daily; for 14 consecutive days) significantly reduces bone marrow leukemia burden in two patient-derived xenograft models of acute myeloid leukemia in NBSGW mice[1].
SSI-4 (30 mg/kg; p.o.; once daily for 1 consecutive week) impairs the early development of B cells in mouse bone marrow, inhibits germinal center formation and immune-induced antigen-specific IgG/IgG1 production; in the influenza infection model of C57BL/6 mice, this agent also suppresses the formation of antiviral germinal centers and the production of IgG/IgG1/IgG2c, while exacerbating weight loss in mice[2].
SSI-4 (60-600 mg/kg; p.o.; consecutive administration; 4.5 weeks) dose-dependently inhibits the growth of subcutaneously inoculated A498 clear cell renal cell carcinoma tumors in athymic nude mice[4].
SSI-4 (20 mg/kg; p.o.; consecutive dosing; 28 days) significantly reduces the pulmonary metastatic tumor burden of ACHN clear cell renal cell carcinoma in athymic nude mice[4].

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

Animal Model: NBSGW[1]
Dosage: 10 mg/kg
Administration: p.o.; daily; 9 days
Result: Significantly prolonged overall survival of mice compared to controls, with a marked separation in survival curves starting around day 30.
Animal Model: NBSGW[1]
Dosage: 10 mg/kg
Administration: p.o.; daily; 14 days
Result: Caused a significant decrease in relative BM leukemia burden in both PDX models, with a more pronounced effect observed in one of the two samples.\n
Induced lipid peroxidation in leukemic cells from treated mice in both models.
Animal Model: C57BL/6 (2-4 months old, both sexes)[2]
Dosage: 30 mg/kg
Administration: oral; daily continuous via chow; 1 week (maintained during immunization or infection period as applicable)
Result: Reduced frequencies of immature B cells, CD19+B220int B cell precursors, and CD25+ pre-B cells in bone marrow; slightly increased mature B cell frequency in peripheral tissues; showed no effect on thymocyte, peripheral CD4+ T cell, or mature peripheral B cell composition.\n
Reduced serum oleic acid and palmitoleic acid content; reduced germinal center B cell frequency from 5.68% to 2.52% and NP+ germinal center B cell frequency from 33.6% to 17.4%; showed no effect on B220intCD138+ plasmablast or PD-1+CXCR5+ Tfh cell frequencies; reduced serum anti-NP IgG.\n
Caused more severe weight loss
Animal Model: Athymic nude mice[4]
Dosage: 60 mg/kg; 180 mg/kg; 600 mg/kg
Administration: oral (incorporated into chow); continuous; 4.5 weeks
Result: Produced dose-dependent inhibition of A498 tumor growth.
Animal Model: Athymic nude mice[4]
Dosage: 180 mg/kg (stated); 20 mg/kg (effective, corrected for altered consumption)
Administration: oral (incorporated into chow); continuous; 28 days
Result: Reduced mean total lung bioluminescent flux.
Reduced mean lesion width of metastatic nodules.
Molecular Weight

388.85

Formula

C19H21ClN4O3
CAS No.
Appearance

Solid

Color

White to off-white

SMILES

O=C(NC)C1=CC(NC(N2CCC(OC3=CC=CC=C3Cl)CC2)=O)=NC=C1
Shipping

Room temperature in continental US; may vary elsewhere.
Storage
Powder -20°C 3 years
4°C 2 years
In solvent -80°C 6 months
-20°C 1 month
Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (257.17 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.5717 mL 12.8584 mL 25.7169 mL
5 mM 0.5143 mL 2.5717 mL 5.1434 mL
View the Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

  • Molarity Calculator

  • Dilution Calculator

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass
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Volume
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Molecular Weight *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start)

C1

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C2

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V2

In Vivo:

Select the appropriate dissolution method based on your experimental animal and administration route.

For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for in vivo experiments, it is recommended to prepare freshly and use it on the same day.
The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.

  • Protocol 1

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: 2.5 mg/mL (6.43 mM); Clear solution; Need ultrasonic

    This protocol yields a clear solution of 2.5 mg/mL.

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.

    Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
  • Protocol 2

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: 2.5 mg/mL (6.43 mM); Clear solution; Need ultrasonic

    This protocol yields a clear solution of 2.5 mg/mL.

    Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

    Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:

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(per animal)

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Number of animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
%
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% 
+
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Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Calculation results:
Working solution concentration: mg/mL
Method for preparing stock solution: mg drug dissolved in μL  DMSO (Stock solution concentration: mg/mL).
The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only. If necessary, please contact MedChemExpress (MCE).
Method for preparing in vivo working solution for animal experiments: Take μL DMSO stock solution, add μL . μL , mix evenly, next add μL Tween 80, mix evenly, then add μL Saline.
 If the continuous dosing period exceeds half a month, please choose this protocol carefully.
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Purity & Documentation

Purity: 99.99%

SDS (254 KB)

COA (248 KB) HNMR (145 KB) RP-HPLC (224 KB) MS (72 KB)

Handling Instructions (2659 KB)
References

Complete Stock Solution Preparation Table

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 2.5717 mL 12.8584 mL 25.7169 mL 64.2921 mL
5 mM 0.5143 mL 2.5717 mL 5.1434 mL 12.8584 mL
10 mM 0.2572 mL 1.2858 mL 2.5717 mL 6.4292 mL
15 mM 0.1714 mL 0.8572 mL 1.7145 mL 4.2861 mL
20 mM 0.1286 mL 0.6429 mL 1.2858 mL 3.2146 mL
25 mM 0.1029 mL 0.5143 mL 1.0287 mL 2.5717 mL
30 mM 0.0857 mL 0.4286 mL 0.8572 mL 2.1431 mL
40 mM 0.0643 mL 0.3215 mL 0.6429 mL 1.6073 mL
50 mM 0.0514 mL 0.2572 mL 0.5143 mL 1.2858 mL
60 mM 0.0429 mL 0.2143 mL 0.4286 mL 1.0715 mL
80 mM 0.0321 mL 0.1607 mL 0.3215 mL 0.8037 mL
100 mM 0.0257 mL 0.1286 mL 0.2572 mL 0.6429 mL
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SSI-4 Related Classifications

Help & FAQs
  • Do most proteins show cross-species activity?

    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.

Keywords:

SSI-41875084-68-6SSI4SSI 4Stearoyl-CoA Desaturase (SCD)DNA/RNA SynthesisApoptosisAutophagymTORInfluenza VirusMammalian target of RapamycinMOLM-13mouse bone marrowMV-4-11acute myeloid leukemiastearoyl-CoA desaturase (SCD1)influenza-infected micepatient-derived xenograft modelshepatocellular carcinomaAML cellsB cellsInhibitorinhibitorinhibit

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