YX968
Based on 1 publication(s) in Google Scholar
YX968 is a selective HDAC3/HDAC8 PROTAC dual degrader, with a DC50 value of 1.7 nM against HDAC3 and 6.1 nM against HDAC8. YX968 inhibits cancer cell growth, induces apoptosis, prevents global histone hyperacetylation, and exerts effects via antiproliferative activity. YX968 can be used in research related to triple-negative breast cancer, non-small cell lung cancer, and multiple myeloma.
(Pink: HDAC3 and hHDAC8 ligand (HY-168287); Blue: VHL ligand (HY-112078); Black: linker (HY-W007700)).
For research use only. We do not sell to patients.
- Purity : 98.06%
- CAS No.: 2742732-92-7
- Formula: C45H66N8O5S
- Molecular Weight:831.12
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Storage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Publications Citing Use of MedChemExpress (MCE) YX968
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Biological Activity
Description
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HDAC3 1.7 nM (DC50) |
HDAC8 6.1 nM (DC50) |
In Vitro
YX968 (8-100 nM; 2-10 h) induce dose- and time-dependent degradation of HDAC3 and HDAC8 in MDA-MB-231 TNBC cells, with effective activity at concentrations as low as 8 nM[1].
YX968 (100 nM) achieves efficient loading into EVs via μDES electroporation, with the loaded EVs maintaining high loading stability across multiple storage conditions, though fresh EVs are optimal due to aggregation-related concentration loss[2].
YX968 forms strong ternary complexes with both purified HDAC3-VHL and HDAC8-VHL protein pairs in an in vitro cell-free system[3].
YX968 (30 min) inhibits purified human HDAC1, HDAC3, and HDAC8 enzymes with micromolar potency, and its inhibitory activity against HDAC3 and HDAC8 is enhanced in the presence of the VHL complex[4].
YX968 (0.1-100000 nM; 45 min) selectively forms stable ternary complexes with purified human HDAC3 and HDAC8 (but not HDAC1) and the VHL-elongin B-elongin C complex, with peak formation at 10 nM[4].
YX968 (8-800 nM; 2-10 h) selectively and potently degrades HDAC3 and HDAC8 in MDA-MB-231 cells, with μDES-loaded EV formulations enhancing this degradative activity compared to other delivery methods, achieving maximum degradation within 10 hrs of treatment[2].
YX968 (16-250 nM; 8 h) is an HDAC3/HDAC8 dual degrader that achieves 91.7% HDAC8 and 94.3% HDAC3 degradation in MDA-MB-231 cells at 16 nM (8 h incubation), and >95% degradation of both isoforms at 250 nM (8 h incubation)[3].
YX968 (100 nM; 2 h) induces degradation of both HDAC3 and HDAC8 in MDA-MB-231 cells when treated with 100 nM for 2 h, as confirmed by TMT-based proteomic profiling[3].
YX968 induces strong antiproliferative activity in MDA-MB-231 cells via dual degradation of HDAC3 and HDAC8, which is more potent than targeting either isoform individually[3].
YX968 (0.063 nM-64 μM; 2-24 h) potently and selectively degrades HDAC3 and HDAC8 in MDA-MB-231 cells via the ubiquitin-proteasome system, with DC50 values of 1.7 nM for HDAC3 and 6.1 nM for HDAC8 after 8 h treatment, and the degradation is reversible upon drug washout[4].
YX968 (14 h) selectively degrades HDAC3 and HDAC8 in MCF7 cells, with histone acetylation induction only at concentrations far higher than those needed for target degradation[4].
YX968 (100 nM; 2 h) induces selective downregulation of HDAC8 and NCOR1 in MDA-MB-231 cells, with no significant off-target protein degradation detected across >7,000 quantified proteins[4].
YX968 (50 nM; 3 h) induces selective downregulation of HDAC3 and NCOR1 (along with three other low-fold-change proteins) in MM.1S cells, with no significant off-target protein degradation detected across ~6,400 quantified proteins[4].
YX968 (3-50 nM; 6-24 h)-mediated degradation of HDAC3 and HDAC8 in MDA-MB-231 cells does not cause significant transcriptomic perturbation, in stark contrast to the broad gene expression changes induced by pan-class I HDAC inhibition[4].
YX968 (125 nM-3 μM; continuous incubation until colony formation) potently suppresses clonogenic growth of multiple breast and lung cancer cell lines, with greater efficacy than HDAC3/HDAC8 inhibitors alone or in combination, and greater potency than HDAC3-selective PROTAC XZ9002[4].
YX968 (0.063-64 μM; 16 h) induces dose-dependent apoptotic cell death in MDA-MB-231 cells via caspase 3 activation, with p21 induction and histone hyperacetylation occurring at higher concentrations than those needed for HDAC3/HDAC8 degradation[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
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Cell Line:MDA-MB-231 human triple negative breast cancer (TNBC) cells
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Concentration:8 nM; 16 nM; 100 nM
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Incubation Time:2 h; 4 h; 6 h; 8 h; 10 h
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Result:Induced HDAC3 degradation in MDA-MB-231 cells at 8 nM, a lower concentration than required for free YX968.
Caused significant dose-dependent degradation of both HDAC3 and HDAC8 at 16 nM and 100 nM.
Started degradative effects as early as 2 h post-treatment, with maximum HDAC3 and HDAC8 degradation observed within 10 h.
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Cell Line:MDA-MB-231 human triple negative breast cancer cells
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Concentration:8-800 nM (degradation assay); 16-100 nM (EV loading concentration)
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Incubation Time:8 h (fixed-time degradation assay); 2-10 h (time-course analysis)
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Result:Induced significant HDAC3/8 degradation at 800 nM when used alone or loaded into EVs via incubation, lipofection, or cuvette-based electroporation.
Maintained HDAC3/8 degradation activity at 8 nM only when loaded into EVs via electroporation.
Increased HDAC3/8 degradation with increasing loading concentration from 16 nM to 100 nM, with the highest EV concentration yielding the greatest HDAC8 degradation.
Showed higher HDAC3/8 degradation efficacy when loaded into μDES-produced EVs than conventional electroporation-produced EVs.
Induced HDAC3/8 degradation as early as 2 hrs post-treatment via μDES-produced EVs, with maximum degradation observed within 10 hrs and no reversal of effects detected.
Exhibited stronger HDAC3 degradation when loaded into EVs via cuvette-based electroporation than via lipofection.
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Cell Line:MDA-MB-231 human triple-negative breast cancer cells
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Concentration:16 nM, 250 nM
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Incubation Time:8 h
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Result:Degraded 91.7% of HDAC8 and 94.3% of HDAC3 at 16 nM.
Achieved >95% degradation of both HDAC8 and HDAC3 at 250 nM.
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Cell Line:MDA-MB-231 triple-negative breast cancer cells
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Concentration:1-16 nM (14 h incubation); 1.7 nM, 6.1 nM (8 h incubation for DC50 determination); 16 nM (washout experiment); 0.063-64 μM (16 h incubation); 100 nM (2 h incubation); 30 nM (14 h incubation); 50 nM (24 h incubation)
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Incubation Time:8 h (DC50 determination); 14 h; 16 h; 24 h; 2 h; 0-24 h (drug-free culture after 24 h treatment)
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Result:Degraded HDAC3 with a DC50 of 1.7 nM and HDAC8 with a DC50 of 6.1 nM after 8 h treatment.
Caused ~75% reduction of HDAC3 at 1 nM; caused >90% reduction of HDAC3 at 16 nM.
Initiated degradation within 1 h, reaching maximum by 4 h.
Led to HDAC3 recovery to 72% and HDAC8 recovery to 84% of steady-state levels by 24 h after washout.
Blocked degradation by proteasome inhibitors (MG132 at 10 μM, bortezomib), neddylation inhibitor MLN4924, and VHL ligand VH032; MG132 at 3 μM only moderately reversed HDAC3 degradation.
Showed no effect on degradation with autophagy inhibitors (3-methyladenine, bafilomycin A1).
Observed no hook effect up to 1 μM, but a hook effect at 64 μM for both HDAC3 and HDAC8.
Did not degrade HDAC1, HDAC2, or HDAC6 at any tested concentration.
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Cell Line:MCF7, T47D, BT549, MDA-MB-468, HCC1806, MDA-MB-231, A549, H1299 cancer cell lines
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Concentration:125 nM; sub-μM concentrations; 3 μM (comparative XZ9002 testing)
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Incubation Time:continuous incubation until colony formation (15-20 days total)
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Result:Effectively inhibited growth of estrogen receptor-positive breast cancer cell lines (MCF7, T47D) and triple-negative breast cancer cell lines (BT549, MDA-MB-468, HCC1806) at 125 nM.
Showed effective growth suppression of MDA-MB-231 and A549 cells at sub-μM concentrations.
Showed no effect on H1299 cells (resistant).
Demonstrated YX968-NC was 2-4-fold less potent than YX968.
Was significantly more potent than HDAC3-selective inhibitor RGFP-966, HDAC8-selective inhibitor PCI 34051, or their combination, and more potent than first-generation HDAC3 PROTAC XZ9002.
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Cell Line:MDA-MB-231 triple-negative breast cancer cells
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Concentration:0.063-64 μM; 10 μM birinapant
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Incubation Time:16 h
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Result:Induced dose-dependent cleavage (activation) of effector caspase 3, with weak activation detectable at 63 nM.
Induced dose-dependent accumulation of p21 and H3K27ac, with weak induction detectable at 63 nM for H3K27ac and 250 nM for p21.
In Vivo
YX968 (100 nM; 1.4×106 EVs/mL; i.p.; 3×/week; ~5 weeks)-loaded EVs delivered via µDES significantly enhance intratumoral HDAC8 degradation and reduce tumour growth in BT-549 TNBC xenograft mice[1].
YX968 (100 nM; 1.4×106 EVs/mL; i.p.; single dose)-loaded EVs delivered via µDES induce targeted, time-dependent degradation of HDAC3 and HDAC8 in human MDA-MB-231 tumours, with no off-target effects in murine PY8119 tumours or spleen tissue in a multi-tumour TNBC mouse model[1].
μDES-produced YX968-loaded EVs (100 nM; intraperitoneal injection; 3 times per week; nearly 5 weeks) deliver significant in vivo HDAC3/HDAC8 degradation in MDA-MB-231 TNBC tumors, reduce tumor growth, and extend mouse median survival by 4.5 days compared to controls[2].
μDES-produced YX968-loaded EVs (100 nM; intraperitoneal injection; single dose) distribute to MDA-MB-231 TNBC tumors in a multi-tumor mouse model, inducing selective HDAC3/8 degradation in human tumors without off-target effects in the spleen or murine tumors[2].
YX968-loaded EVs (1000 nM; 1.4×1011 EVs/mL; i.p.; 2 doses (Day 0 and Day 7)) delivered via µDES exhibit a safe in vivo profile with no detectable toxicity in healthy C57BL/6J mice[1].
High-dose μDES-produced YX968-loaded EVs (1000 nM; intraperitoneal injection; 2 doses on days 0 and 7) are well-tolerated in healthy C57BL/6J mice, with no observed body weight loss, hematological abnormalities, or tissue damage, unlike YX968 alone which causes kidney and liver toxicity[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:NOD-SCID interleukin-2 receptor gamma null (NSG) mice[1]
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Dosage:100 nM (starting concentration); 1.4×1010 EVs/mL
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Administration:i.p.; 3×/week; ~5 weeks
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Result:Reduced tumour size and growth rate significantly compared to free YX968, unloaded EVs, or PBS controls.
Extended mouse survival to 39 days, compared to 30 days for the free YX968 group (p < 0.0005).
Induced significant degradation of HDAC3 and HDAC8 in tumour lysates; free YX968 did not induce significant HDAC degradation in tumours.
Detected no HDAC degradation in spleen tissue.\nReduced tumour size significantly compared to free YX968 controls.
Induced significant degradation of HDAC8 in tumour lysates; free YX968 did not induce significant HDAC degradation in tumours.
Detected no HDAC degradation in spleen tissue.
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Animal Model:NOD-SCID interleukin-2 receptor gamma null (NSG) mice[1]
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Dosage:100 nM (starting concentration); 1.4×1010 EVs/mL
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Administration:i.p.; single dose
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Result:Induced significant degradation of HDAC3 and HDAC8 in MDA-MB-231 tumours at 15 and 24 hours post-injection.
Did not induce noticeable HDAC degradation in MDA-MB-231 tumours for free YX968 and unloaded EVs.
Detected no HDAC degradation in PY8119 tumours or spleen tissue across any treatment group or time point.
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Animal Model:C57BL/6J mice (male and female, 7-9 weeks old)[1]
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Dosage:1000 nM (starting concentration); 1.4×1011 EVs/mL
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Administration:i.p.; 2 doses (Day 0 and Day 7)
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Result:Observed no decline in body weight in any treatment group.
Detected no significant changes in haematological parameters (white blood cells, lymphocytes, neutrophils, red blood cells, platelets).
Showed no tissue damage or toxicity in kidney, liver, and small intestine via histological analysis.
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Animal Model:NOD-SCID interleukin-2 receptor gamma null (NSG) (age 7-9 weeks, subcutaneous implantation of 1 × 106 MDA-MB-231 human breast cancer cells)[2]
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Dosage:100 nM YX968 loaded into EVs at a concentration of 1.4 × 1010 EVs/mL
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Administration:intraperitoneal injection; 3 times per week; nearly 5 weeks
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Result:Reduced final tumor volume significantly compared to vehicle, unloaded EV, and YX968-only groups.
Induced considerable HDAC3/8 degradation in tumors.
Prolonged median survival time by 4.5 days compared to control groups.
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Animal Model:NOD-SCID interleukin-2 receptor gamma null (NSG) (age 7-9 weeks, subcutaneous implantation of 1 × 106 MDA-MB-231 human breast cancer cells and 5 × 105 PY8119 murine breast cancer cells)[2]
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Dosage:100 nM YX968 loaded into EVs at a concentration of 1.4 × 1010 EVs/mL
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Administration:intraperitoneal injection; single dose
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Result:Showed strong fluorescent signal in vivo for up to 48 hours post-injection.
Accumulated primarily in spleen, liver, and both tumors in ex vivo imaging.
Induced HDAC3/8 degradation in MDA-MB-231 tumors at 15 and 24 hours post-injection.
Caused no HDAC3/8 degradation in spleen or PY8119 tumors at any time point.
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Animal Model:C57BL/6J (age 7-9 weeks, both male and female)[2]
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Dosage:1000 nM YX968 loaded into EVs at a concentration of 1.4 × 1011 EVs/mL
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Administration:intraperitoneal injection; 2 doses on days 0 and 7
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Result:Caused no decline in body weight in male or female mice.
Kept hematological parameters (white blood cells, lymphocytes, neutrophils, red blood cells, platelets) relatively unchanged compared to controls.
Showed no observable tissue damage to kidney, liver, or small intestine.
Chemical Information
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CAS No. 2742732-92-7
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Appearance Solid
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Molecular Weight 831.12
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Formula C45H66N8O5S
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Color White to off-white
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SMILES
CCCNNC(C(C=C1)=CC=C1N(CC2)CCN2CCCCCCCC(N[C@@H](C(C)(C)C)C(N3[C@@H](C[C@H](C3)O)C(N[C@H](C4=CC=C(C5=C(N=CS5)C)C=C4)C)=O)=O)=O)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month
Publications (1)
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Journal Impact Factor
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Most Recent
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Sci Adv
2026 Apr 10;12(15):eaec0149. PMID: 41961925
Solvent & Solubility
In Vitro:
DMSO : 100 mg/mL (120.32 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
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.
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.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: 5 mg/mL (6.02 mM); Clear solution; Need ultrasonic and warming and heat to 60°C
This protocol yields a clear solution of 5 mg/mL.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 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.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: 5 mg/mL (6.02 mM); Clear solution; Need ultrasonic and warming and heat to 60°C
This protocol yields a clear solution of 5 mg/mL.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (50.0 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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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%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
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
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.
Protocols
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Protocol for Cell Counting and Cell Density Analysis
Cell counting and cell-density analysis estimate the number of cells in a known volume or field area. Manual hemocytometer counting uses a chamber of defined geometry to convert counted cells into cells/mL, while automated counters and image-analysis workflows detect cell objects from optical, brightfield, fluorescence, impedance, or digital-image features. Trypan blue viability counting is based on dye exclusion: viable cells with intact membranes exclude dye, while non-viable cells with compromised membranes stain blue. The readout is total cell density, viable-cell density, dead-cell density, and percent viability. Cell density can also be estimated from microscopy images by counting objects per image area, from flow cytometry using calibrated volume or reference particles, or from in situ microscopy in bioreactors after calibration against reference methods such as hemocytometer or flow cytometry.
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Somatic Cell Culture
A method of simulating the in vivo environment in vitro to maintain the cell growth, differentation and main functions.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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CCK-8/WST-8 Cell Proliferation Assay
The CCK-8/WST-8 assay is based on the reduction of the water-soluble tetrazolium salt WST-8 to a water-soluble formazan product by cellular dehydrogenases in metabolically active cells, where the generated formazan amount is proportional to the number of living cells and is quantified by measuring absorbance in the visible range, providing a colorimetric readout for cell viability and proliferation assessment. This class of tetrazolium-based assays improves upon earlier MTT-based systems by producing a water-soluble formazan, eliminating the need for organic solubilization steps and enabling direct spectrophotometric measurement in culture medium.
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Cell Counting-Based Growth Curve Assay
Cell counting-based growth curve assays quantify cell proliferation by directly measuring changes in viable cell number over time using manual or automated counting methods such as hemocytometer-based counting or instrument-assisted cell enumeration, enabling construction of growth curves that reflect population expansion dynamics in response to culture conditions. A widely used approach is trypan blue exclusion with hemocytometer counting, where membrane-compromised (non-viable) cells take up the dye, allowing discrimination between viable and non-viable cells while simultaneously enabling total cell number quantification. Repeated sampling across time points allows estimation of proliferation rate, growth phases, and comparative growth kinetics between experimental conditions.
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MTT Cell Proliferation Assay
The MTT assay is a colorimetric endpoint assay for estimating viable cell number, cell growth, cytotoxicity, or cell activation in cultured mammalian cells. Living cells reduce the yellow tetrazolium salt MTT into purple/blue formazan, while dead cells do not generate the same signal; the resulting color can be quantified with a multiwell spectrophotometer. MTT reduction is commonly interpreted as a readout of metabolic activity that often correlates with viable cell number, but it should not be treated as a direct cell-counting method unless the assay is optimized for the cell type and experimental condition. Studies show that MTT reduction can involve mitochondrial and non-mitochondrial reducing systems, and formazan may accumulate in intracellular lipid droplets rather than simply marking mitochondria.
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Breast Cancer Modeling
Breast cancer is a heterogeneous cancer, and it has been distinguished into four subtypes: luminal A, luminal B, HER2-positive and basal-like. Molecular mutations, epigenetic alterations, hormone exposure and immune microenvironment are related to the progression of breast cancer.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
Purity & Documentation
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Data Sheet (294 KB)
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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)
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Handling Instructions (2659 KB)
References
[1]. Erwin N, et al. Proteolysis Targeting Chimera Loaded Extracellular Vesicles for Developing Triple Negative Breast Cancer Treatment. Journal of extracellular vesicles. 2025 Dec;14(12):e70211. [Content Brief]
[3]. Xiao Y, et al. Discovery of a Highly Potent and Selective HDAC8 Degrader: Advancing the Functional Understanding and Therapeutic Potential of HDAC8. Journal of medicinal chemistry. 2024 Aug 08;67(15):12784-12806. [Content Brief]
[4]. Xiao Y, et al. HDAC3 and HDAC8 PROTAC dual degrader reveals roles of histone acetylation in gene regulation. Cell chemical biology. 2023 Nov 16;30(11):1421-1435.e12. [Content Brief]
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 | 1.2032 mL | 6.0160 mL | 12.0320 mL | 30.0799 mL |
| 5 mM | 0.2406 mL | 1.2032 mL | 2.4064 mL | 6.0160 mL | |
| 10 mM | 0.1203 mL | 0.6016 mL | 1.2032 mL | 3.0080 mL | |
| 15 mM | 0.0802 mL | 0.4011 mL | 0.8021 mL | 2.0053 mL | |
| 20 mM | 0.0602 mL | 0.3008 mL | 0.6016 mL | 1.5040 mL | |
| 25 mM | 0.0481 mL | 0.2406 mL | 0.4813 mL | 1.2032 mL | |
| 30 mM | 0.0401 mL | 0.2005 mL | 0.4011 mL | 1.0027 mL | |
| 40 mM | 0.0301 mL | 0.1504 mL | 0.3008 mL | 0.7520 mL | |
| 50 mM | 0.0241 mL | 0.1203 mL | 0.2406 mL | 0.6016 mL | |
| 60 mM | 0.0201 mL | 0.1003 mL | 0.2005 mL | 0.5013 mL | |
| 80 mM | 0.0150 mL | 0.0752 mL | 0.1504 mL | 0.3760 mL | |
| 100 mM | 0.0120 mL | 0.0602 mL | 0.1203 mL | 0.3008 mL |
YX968 Related Classifications
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