Cat. No.: HY-162008

S1g-10

Name: S1g-10
Brand: MedChemExpress
SKU: HY-162008
Price: 600.00 USD
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S1g-10 is an Hsp70-Bim protein-protein interaction inhibitor and an Hsp70 ATPase inhibitor. S1g-10 binds the Hsp70 nucleotide-binding domain at the Bim interface, inhibits Bim-stimulated ATPase activity, and selectively disrupts Hsp70-Bim without affecting Hsp70-Bag3, thereby inhibiting mitophagy (Autophagy), inducing apoptosis (Apoptosis), and reducing the survival and self-renewal of CML leukemia stem cells. S1g-10 can be used for research on chronic myeloid leukemia and breast cancer.

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

Purity : 99.08%
CAS No.: 3032432-71-3
Formula: C₂₆H₃₁N₃OS
Molecular Weight:433.61

Storage:

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

S1g-10 Chemical Structure

CAS No.: 3032432-71-3

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Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Solvent & Solubility
- In Vitro
- In Vivo
Purity & Documentation
References
Help & FAQs
Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target

^[4]

HSP70

688 nM (Kd)

All HSP Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
BV-173	EC50	0.62 μM	Apoptosis induction against human CML BV173 cells assessed by Annexin V-FITC staining. Apoptosis induction against human CML BV173 cells assessed by Annexin V-FITC staining.	38011535
K562	EC50	1.3 μM	Apoptosis induction against human CML K562 cells assessed by Annexin V-FITC staining. Apoptosis induction against human CML K562 cells assessed by Annexin V-FITC staining.	38011535
K562	EC50	0.34 μM	Apoptosis induction against human TKI-resistant CML K562-R3 cells assessed by Annexin V-FITC staining. Apoptosis induction against human TKI-resistant CML K562-R3 cells assessed by Annexin V-FITC staining.	38011535
MDA-MB-231	IC50	14.9 μM	Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human MDA-MB-231 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
BT-549	IC50	16.7 μM	Cytotoxicity against human BT549 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human BT549 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
MCF7	IC50	27.0 μM	Cytotoxicity against human MCF7 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human MCF7 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
SK-BR-3	IC50	24.2 μM	Cytotoxicity against human SKBR3 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human SKBR3 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
CAMA-1	IC50	19.0 μM	Cytotoxicity against human CAMA1 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human CAMA1 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
T47D	IC50	22.3 μM	Cytotoxicity against human T47D breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human T47D breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
MDA-MB-468	IC50	16.0 μM	Cytotoxicity against human MDA-MB-468 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human MDA-MB-468 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
MDA-MB-157	IC50	15.4 μM	Cytotoxicity against human MDA-MB-157 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human MDA-MB-157 breast cancer cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
HEK-293T	IC50	> 30 μM	Cytotoxicity against human embryonic kidney HEK-293T cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay. Cytotoxicity against human embryonic kidney HEK-293T cells assessed as viability reduction after 48 hrs incubation by CCK-8 assay.	40938081
BV-173	EC50	0.66 μM	Induction of apoptosis in human CML BV173 cells after incubation with S1g-10 for 48 hrs assessed by Annexin V-FITC flow cytometry. Induction of apoptosis in human CML BV173 cells after incubation with S1g-10 for 48 hrs assessed by Annexin V-FITC flow cytometry.	39012838
K562	EC50	1.20 μM	Induction of apoptosis in human CML K562 cells after incubation with S1g-10 for 48 hrs assessed by Annexin V-FITC flow cytometry. Induction of apoptosis in human CML K562 cells after incubation with S1g-10 for 48 hrs assessed by Annexin V-FITC flow cytometry.	39012838
K562	EC50	0.37 μM	Induction of apoptosis in human CML TKI-resistant K562-R3 cells after incubation with S1g-10 for 48 hrs assessed by Annexin V-FITC flow cytometry. Induction of apoptosis in human CML TKI-resistant K562-R3 cells after incubation with S1g-10 for 48 hrs assessed by Annexin V-FITC flow cytometry.	39012838

In Vitro

S1g-10 (1 μM; week 1 of a 6-week culture; colonies counted after 14 days) reduces LTC-IC colony formation by 50%-70% in CML#1 CD34⁺CD38⁻ cells without affecting healthy donor CD34⁺CD38⁻ cells^[1].
S1g-10 (1 μM; 6-24 h) does not change the levels of AKT, eIF4E, or Raf-1 in CML#1 CD34⁺ cells, but decreases these proteins in CD34⁻ differentiated CML cells^[1].
S1g-10 (1 μM; 24 h) upregulates hematopoietic lineage/differentiation markers, including CD11b, CD48, and CD71, in CML#3 CD34⁺ cells^[1].
S1g-10 (1 μM; 3 days) reduces the absolute number of CD34⁺CD38⁻ LSCs in CML#2-5, while no additional effect is observed in cells exposed to BafA1^[1].
S1g-10 perturbs Hsp70−Bim signaling in K562 cells and reduces the expression/phosphorylation of AKT and EIF4e^[2].
S1g-10 (48 h) inhibits the viability of MDA-MB-231, BT549, MCF7, SKBR3, CAMA1, T47D, MDA-MB-468, and MDA-MB-157 breast cancer cells with IC₅₀ values of 14.9, 16.7, 27.0, 24.2, 19.0, 22.3, 16.0, and 15.4 µM, respectively, whereas the IC₅₀ in HEK-293T cells is > 30 µM^[3].
S1g-10 (3 μM; 12 hours) selectively disrupts the Hsp70-Bim PPI in K562 cells without affecting Hsp70-Bag3^[4].
S1g-10 prevents SB-2-mediated BRD4 degradation in U-87 MG cells by competing with Hsp70 and disrupting the BRD4-Hsp70TAC-Hsp70 ternary complex^[5].
S1g-10 blocks SP-2-induced PD-L1 degradation in MDA-MB-231 cells by competing with Hsp70 and preventing the formation of the PD-L1-Hsp70TAC-Hsp70 ternary complex^[5].
S1g-10 (2 µM; 12 hours) does not inhibit Bcr-Abl Y412 phosphorylation in K562R cells^[6].
S1g-10 (10 µM; 12 hours) does not disrupt the Hsp70-Bcr-Abl interaction in K562R cells^[6].
S1g-10 (50 µM) inhibits the Bcr-Abl DBD-enhanced Hsp70 ATPase activity in K562R shBcr-Abl and HL-60 cell lysates^[6].
S1g-10 (2 µM; 12 hours) disrupts Hsp70-Bim, Hsp70-AKT, and Hsp70-eIF4E interactions and reduces AKT/eIF4E levels in K562R shBcr-Abl/DBD cells^[6].
S1g-10 (2 µM; 12 h) prevents the restoration of Bcr-Abl DBD-dependent nuclear export of MYC and survivin in K562R cells^[6].
S1g-10 (48 h) selectively induces apoptosis in CML cells, including TKI-resistant K562-R3, with an EC₅₀ of 0.37 μM, without affecting HEK293 and BaF3 cells^[4].
S1g-10 (2 µM) restores apoptosis in K562R/K562 cells expressing Bcr-Abl DBD^[6].
S1g-10 (1 μM; 12 h) inhibits autophagy more strongly in primary CML CD34⁺ stem/progenitor cells than in CD34⁻ differentiated CML cells^[1].
S1g-10 (1 μM; 24 h) increases CD11b and E2F2 in CML#3 CD34⁺ cells, which depends on the inhibition of mitophagy^[1].
S1g-10 (1 μM; 12 h) inhibits mitophagy in Bcr-Abl-expressing BaF3 and K562 cells, but not in Bcr-Abl-negative or Bcr-Abl-knockdown cells^[1].
S1g-10 (1 μM) reduces the colocalization of LC3 with mitochondria in CML LSCs^[1].
S1g-10 (1 μM; 24 h) decreases the G0 phase proportion and increases the S-G2-M phase in CML LSCs, indicating loss of quiescence^[1].
S1g-10 induces apoptosis in BV173, K562, and K562-R3 CML cells with EC₅₀ values of 0.34-1.3 μM, and does not affect HEK293 and BaF3 cells^[2].
S1g-10-induced apoptosis in K562 cells depends on Hsp70 and Bim, supporting the inhibition of Hsp70−Bim PPI targeting^[2].
S1g-10 (0-100 µM; 30 minutes) inhibits the single-turnover ATPase activity of recombinant GRP75, GRP78, and HSP70, with IC₅₀ values in the low micromolar range^[3].
S1g-10 (1-5 µM; 6 hours) selectively modulates cytosolic HSP70-Bim signaling in HeLa cells and downregulates AKT/eIF4E at 1 µM, while not affecting GRP75- or GRP78-mediated pathways at 5 µM^[3].
S1g-10 (1 μM; 12 h) increases mitochondrial proteins 2-3 fold in CML#2 CD34⁺ cells and selectively does not affect ER proteins^[1].
S1g-10 (50 µM; 30 minutes) exhibits lower subcellular accumulation in isolated mitochondria and ER than the organelle-targeted derivatives 5 and 8^[3].
S1g-10 (1 μM; 12 h) increases mitochondrial content by approximately 7-fold in CML#2 CD34⁺CD38⁻ LSCs and by approximately 1.5-fold in differentiated CML cells, and does not affect healthy HSCs^[1].
S1g-10 (5 µM; 30 minutes) shows no obvious colocalization with Mito-Tracker Red or ER-Tracker Red in HeLa cells^[3].
S1g-10 (1 μM; 12 h) increases mitochondrial ROS in primary CML#1-5 CD34⁺ cells^[1].
S1g-10 (compound 21) disrupts the Hsp70−Bim PPI in vitro, K_i = 0.25 μM^[2].
S1g-10 selectively inhibits Bim-stimulated Hsp70 ATPase activity, IC₅₀ = 15.8 μM^[2].
S1g-10 binds the Hsc70 NBD/Hsp70 interface and significantly perturbs Asp225, sharing the binding interface with S1g-2^[2].
S1g-10 (1-5 μM) selectively disrupts the Hsp70−Bim PPI in K562 cells without affecting Hsp70−Bag3^[2].
S1g-10 (10 min) inhibits the Hsp70-Bim PPI in FPA with an IC₅₀ of 0.80 μM^[4].
S1g-10 (0.15 mM) directly binds Hsp70 in ITC with a K_d of 688 nM^[4].
The water solubility of S1g-10 (10 mg dissolved in 1 mL water; 24 hours) is 7.19 μg/mL^[4].
S1g-10 (50 µM) attenuates Bim-stimulated Hsp70 ATPase activity^[6].
S1g-10 (50 µM) eliminates Hsp70/Bim-dependent Rhodanese (HY-P2864) aggregation inhibition^[6].

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

Western Blot Analysis^[1]

Cell Line:

BaF3, Bcr-Abl-transfected BaF3, K562, and Bcr-Abl shRNA-transfected K562 cells
Concentration:

1 μM
Incubation Time:

12 h
Result:

Led to significant inhibition of mitophagy in Bcr-Abl-transformed BaF3 and K562 cells, but not in BaF3 and Bcr-Abl-knockdown K562 cells, as evidenced by accumulations of COX IV and NDUFB8, LC3 conversion, and changes in p62.
In mitochondrial fractions, decreased LC3-II and p62 levels in Bcr-Abl-expressing cells but not in Bcr-Abl-non-expressing cells.
Decreased 561 nm/488 nm mKeima fluorescent ratios in K562 cells.

Western Blot Analysis^[3]

Cell Line:

HeLa cells
Concentration:

1 µM; 5 µM
Incubation Time:

6 h
Result:

Significantly disrupted the HSP70-Bim PPI and downregulated HSP70 clients AKT and eIF4E at 1 µM.
Did not affect the GRP75-p53 interaction and did not increase eIF2α phosphorylation, ATF4, or CHOP expression at 5 µM.

Apoptosis Analysis^[4]

Cell Line:

human CML cell lines K562, BV173, TKI-resistant K562-R3, and human normal HEK293 and BaF3 cells
Concentration:

0.66 μM (BV173 EC₅₀); 1.20 μM (K562 EC₅₀); 0.37 μM (K562-R3 EC₅₀); 15 μM (HEK293/BaF3)
Incubation Time:

48 h
Result:

Induced apoptosis in CML cell lines with EC₅₀ values of 0.66 μM in BV173, 1.20 μM in K562, and 0.37 μM in K562-R3; in HEK293 and BaF3 cells, the apoptotic rate was < 10% at 15 μM.

Western Blot Analysis^[6]

Cell Line:

K562R CML cells
Concentration:

2 µM
Incubation Time:

12 h
Result:

Did not reduce Y412-phosphorylated Bcr-Abl; relative level was 1.1 (DMSO control 1.0).

Real Time qPCR^[6]

Cell Line:

K562R cells
Concentration:

2 µM
Incubation Time:

12 h
Result:

Abolished the Bcr-Abl DBD-dependent restoration of cytoplasmic-to-nuclear ratios of MYC and survivin at 2 µM.

Parmacokinetics

Species	Dose	Route	C_max	T_max	T_1/2	CL	AUC_0-t
Rat^[2]	3 mg/kg	i.p.	2.3 μg/mL	1.0 h	5.2 h	4.1 mL/min/kg	729100 min·ng/mL

In Vivo

S1g-10 (2 mg/kg; i.p.; once daily; 14 days) reduces the number of human CML LSCs in the bone marrow in a long-term human CD34⁺ CML cell xenograft model^[1].
S1g-10 (2.0 mg/kg; i.p.; once daily; 14 days) reduces tumor growth in K562-R1 Imatinib (HY-15463)-resistant CML xenografts in BALB/c nu/nu mice, with T/C = 33.51%^[2].
S1g-10 (2 mg/kg; i.p.; once daily; 5 days) inhibits mitophagy in human CML LSCs within the bone marrow in a short-term human CD34⁺ CML cell xenograft model^[1].

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

Animal Model:

NYG (NOD-Prkdc^em1 Il2rg^em1; female; 7-8 weeks old; sublethally irradiated (2.25 Gy))^[1]
Dosage:

2 mg/kg
Administration:

i.p.; once daily; 5 days
Result:

Inhibited mitophagy in bone marrow-located human CML LSCs, shown by decreased p62/TOMM20 co-localization.
Mitochondria/nuclear ratio was elevated in human CD45⁺CD34⁺CD38⁻ cells from mice compared with vehicle control mice.

Animal Model:

NYG (NOD-Prkdc^em1 Il2rg^em1; female; 7-8 weeks old; sublethally irradiated (2.25 Gy))^[1]
Dosage:

2 mg/kg
Administration:

i.p.; once daily; 14 days
Result:

Quantitative flow cytometry of sorted human CD45⁺ cells from bone marrow showed that CD45⁺CD34⁺CD38⁻ CML cells were nearly completely eradicated in 3 of 5 mice.
In the remaining two mice, 65% and 66% of CD45⁺CD34⁺CD38⁻ CML cells in bone marrow were eliminated.
Reduced the number of LSCs by more than 80% after two weeks of injection.

Animal Model:

BALB/c nu/nu (male, 6 weeks old)^[2]
Dosage:

2.0 mg/kg
Administration:

i.p.; once daily; 14 days
Result:

A reduction in tumor growth and decreased tumor weight were observed compared with vehicle-injected controls (T/C = 33.51%).
Disruption of the Hsp70−Bim PPI and destabilization of oncogenic clients AKT and EIF4e were detected in excised tumors.

Related Protocols :

Chemical Information

CAS No. 3032432-71-3
Appearance Solid
Molecular Weight 433.61
Formula C₂₆H₃₁N₃OS
Color Light yellow to yellow
SMILES

O=C1C(C#N)=C(C2=CC=C(C3=C2C1=CC=C3)SC4CCCCC4)NCCN(CC)CC
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 : 25 mg/mL (57.66 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

2.3062 mL

11.5311 mL

23.0622 mL

5 mM

0.4612 mL

2.3062 mL

4.6124 mL

10 mM

0.2306 mL

1.1531 mL

2.3062 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.

Molarity Calculator

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

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Molecular Weight Molecular Weight

Dilution Calculator

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

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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: ≥ 1 mg/mL (2.31 mM); Clear solution

This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (10.0 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: ≥ 1 mg/mL (2.31 mM); Clear solution

This protocol yields a clear solution of ≥ 1 mg/mL (saturation unknown).

Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (10.0 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.

In Vivo Dissolution Calculator

Please enter the basic information of animal experiments:

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mg/kg
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g
Dosing Volume (Per Animal) Dosing Volume (Per Animal)
μL
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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

Purity & Documentation

Select Batch:

Purity: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (296 KB)
SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 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)

References

[1]. Song T, et al. Hsp70-Bim interaction mediated mitophagy as a potential therapeutic target for CML stem cells. Stem cell reports. 2026 Jan 13;21(1):102751.

[2]. Wang Z, et al. Exploiting the "Hot-Spots" of Hsp70Bim ProteinProtein Interaction to Optimize the 1-Oxo-1-phenalene-2,3-dicarbonitrile Analogues as Specific Hsp70Bim Inhibitors. Journal of medicinal chemistry. 2023 Dec 14;66(23):16377-16387. [Content Brief]

[3]. Jiang M, et al. Revealing GRP75-Mediated Mitochondrial Stability That Promotes Breast Cancer Survival through Subcellular Anchoring of 70 kDa Heat Shock Protein Inhibitors. Journal of medicinal chemistry. 2025 Sep 25;68(18):19169-19183. [Content Brief]

[4]. Jiang M, et al. Discovery of Biphenyl Derivatives to Target Hsp70-Bim Protein-Protein Interaction in Chronic Myeloid Leukemia by Scaffold Hopping Strategy. Journal of medicinal chemistry. 2024 Jul 25;67(14):12068-12084. [Content Brief]

[5]. Wang Z, et al. Hsp70-Targeting Chimeras Enable Dual Proteasomal and Lysosomal Degradation of Intracellular and Extracellular Proteins. Journal of medicinal chemistry. 2026 Apr 09;69(7):8417-8432. [Content Brief]

[6]. Zhang H, et al. A kinase-independent Bcr-Abl function mediating an Hsp70-Bim protein-protein interaction in chronic myeloid leukemia. International journal of biological macromolecules. 2025 May;310(Pt 3):143249. [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	2.3062 mL	11.5311 mL	23.0622 mL	57.6555 mL
	5 mM	0.4612 mL	2.3062 mL	4.6124 mL	11.5311 mL
	10 mM	0.2306 mL	1.1531 mL	2.3062 mL	5.7655 mL
	15 mM	0.1537 mL	0.7687 mL	1.5375 mL	3.8437 mL
	20 mM	0.1153 mL	0.5766 mL	1.1531 mL	2.8828 mL
	25 mM	0.0922 mL	0.4612 mL	0.9225 mL	2.3062 mL
	30 mM	0.0769 mL	0.3844 mL	0.7687 mL	1.9218 mL
	40 mM	0.0577 mL	0.2883 mL	0.5766 mL	1.4414 mL
	50 mM	0.0461 mL	0.2306 mL	0.4612 mL	1.1531 mL

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S1g-10

All HSP Isoforms