Art. -Nr.: HY-155033

SSI-4

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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.

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Reinheit: 99.99%
CAS. Nr.: 1875084-68-6
Formel: C₁₉H₂₁ClN₄O₃
Molecular Weight:388.85

Speicherung:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

SSI-4 Chemical Structure

CAS. Nr.: 1875084-68-6

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Biologische Aktivität
- Beschreibung
- IC₅₀ & Target
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Lösungsmittel & Löslichkeit
- In Vitro
- In Vivo
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

IC₅₀ & Target

SCD1^[1]

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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.

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	C_max	T_1/2	AUC_0-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.

Chemical Information

CAS. Nr. 1875084-68-6
Appearance Solid
Molecular Weight 388.85
Formel C₁₉H₂₁ClN₄O₃
Color White to off-white
SMILES

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

Room temperature in continental US; may vary elsewhere.

Speicherung

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Lösungsmittel & Löslichkeit

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)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

2.5717 mL

12.8584 mL

25.7169 mL

5 mM

0.5143 mL

2.5717 mL

5.1434 mL

10 mM

0.2572 mL

1.2858 mL

2.5717 mL

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.

Molaritätsrechner

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

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

In Vivo:

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

Stock Solution Working Solution

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.

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.

Protocol 3

Add each solvent one by one: 10% DMSO 90% Corn Oil

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

This protocol yields a clear solution of 2.5 mg/mL. If the continuous dosing period exceeds half a month, please choose this protocol carefully.

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (25.0 mg/mL) to 900 μL Corn oil, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

Dosage Dosage
mg/kg
Animal Weight (Per Animal) Animal Weight (Per Animal)
g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
Number of Animals Number of Animals

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.

Please enter your animal formula composition:

%
DMSO +

Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
%
+
+
%
Tween-80 + +
%
Saline +

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).

Working solution concentration: 0.22 mg/mL

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (289 KB)
SDS (254 KB)
- English - EN (254 KB)
- Français - FR (254 KB)
- Deutsch - DE (254 KB)
- Norwegian - NO (254 KB)
- Español - ES (254 KB)
- Swedish - SV (254 KB)
- Italian - IT (254 KB)
- Korean - KR (254 KB)
- Portuguese - PT (254 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Dembitz V, et al. Stearoyl-CoA desaturase inhibition is toxic to acute myeloid leukemia displaying high levels of the de novo fatty acid biosynthesis and desaturation. Leukemia. 2024;38(11):2395-2409. [Content Brief]

[2]. Zhou X, et al. Stearoyl-CoA Desaturase-Mediated Monounsaturated Fatty Acid Availability Supports Humoral Immunity. Cell Rep. 2021;34(1):108601. [Content Brief]

[3]. Li KP, et al. Radiosynthesis and Preliminary Evaluation of [¹¹C]SSI-4 for the Positron Emission Tomography Imaging of Stearoyl CoA Desaturase 1. Mol Pharm. 2023;20(8):4129-4137. [Content Brief]

[4]. von Roemeling CA, et al. Accelerated bottom-up drug design platform enables the discovery of novel stearoyl-CoA desaturase 1 inhibitors for cancer therapy. Oncotarget. 2017;9(1):3-20. Published 2017 Oct 6. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

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

Anti-Infection Compound Library

Apoptosis Compound Library

Cell Cycle/DNA Damage Compound Library

Immunology/Inflammation Compound Library

Kinase Inhibitor Library

Metabolism/Protease Compound Library

PI3K/Akt/mTOR Compound Library

Stem Cell Signaling Compound Library

Anti-Cancer Compound Library

Antiviral Compound Library

Autophagy Compound Library

Anti-Aging Compound Library

Antioxidant Compound Library

Differentiation Inducing Compound Library

Reprogramming Compound Library

Oxygen Sensing Compound Library

Ferroptosis Compound Library

Endoplasmic Reticulum Stress Compound Library

Glycolysis Compound Library

Cytoskeleton Compound Library

Orally Active Compound Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Blood Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Anti-Obesity Compound Library

Angiogenesis-Related Compound Library

Lipid Metabolism Compound Library

Glucose Metabolism Compound Library

Anti-Liver Cancer Compound Library

Anti-Colorectal Cancer Compound Library

Anti-Prostate Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Cancer Stem Cells Compound Library

Pain-Related Compound Library

Mitochondrial Protection Compound Library

Metabolic Enzyme Compound Library

Cell Death Library

Serine/Threonine Kinase Inhibitor Library

Anti-Hematopathy Compound Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Radioprotector Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Bioactive Compound Library

Anti-Gastric Cancer Compound Library

Anti-Fibrosis Compound Library

Anti-Brain Cancer Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

High-Throughput Bioactive Compound Library

Lactylation Compound Library

Alle DNA/RNA Synthesis Isoform-spezifische Produkte anzeigen

Alle mTOR Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise

Help & FAQs

Complete Stock Solution Preparation Table

SSI-4 Related Classifications

HY-155033 Related Classifications