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Fig. 1 · Structure
Cat. No.
A10586
CAS No.
726169-73-9
Formula
C23H20N6O
Mol. Weight
396.4

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Mocetinostat (MGCD0103)

Cat. No. A10586 CAS 726169-73-9

HDAC Inhibitor

MGCD0103 (Mocetinostat) is a benzamide histone deacetylase inhibitor by inhibiting mainly histone deacetylase 1 (HDAC1), but also HDAC2, HDAC3, and HDAC11.

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Publications for Mocetinostat

2 publications citing this product

  1. Mari Ishigami-Yuasa, .et al. , Biol Pharm Bull, 2019, 42, 448-452 PMID: 30828077
  2. Guang Bai, .et al. , Epigenetics of Chronic Pain, 2019, Pages 1-48
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Biological Activity

Bioactivity / Mechanism

A cellular test of the proposed HDAC1/2–Gli1 mechanism found that 0.5 µM mocetinostat reduced proliferation of DAOY cells expressing wild-type Gli1, while cells expressing the non-acetylatable Gli1 K518R mutant showed no significant reduction over 24–48 hours. This supports a role for Gli1 K518 acetylation in this model. The tested material was mocetinostat dihydrobromide. [1]

Literature-reported observations and conditions; not Adooq-tested protocols or general treatment recommendations.

Target & Activity

Target Activity Value
HDAC1 IC50 0.15μM
HDAC2 IC50 0.29μM
HDAC11 IC50 0.59μM
HDAC3 IC50 1.66μM
HDAC4 IC50 >10μM
HDAC5 IC50 >10μM
HDAC6 IC50 >10μM
HDAC7 IC50 >10μM
HDAC8 IC50 >10μM

9 targets · Scroll to view more

In Vitro Studies

In LNCaP prostate cancer cells, the 72-hour growth-inhibition IC50 of MGCD0103 was 0.75 µM alone and 1.4 µM with 25 µM Am80. The authors reported no enhanced growth-inhibitory effect for this combination. These are cell-based growth endpoints, not HDAC enzyme IC50 values. [2]

MGCD0103 did not enhance Am80-associated growth inhibition in LNCaP cells

Cell-based study · Human LNCaP prostate cancer cells [2]

The reported growth-inhibition IC50 was 0.75 µM without Am80 and 1.4 µM with 25 µM Am80 after 72 h. The authors report no enhanced growth-inhibitory effect for MGCD0103. This comparison does not establish formal synergy or antagonism.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
LNCaP growth inhibition without Am80IC50 0.75 µM[2]
LNCaP growth inhibition in the presence of 25 µM Am80IC50 1.4 µM[2]

Literature-Reported Treatment Conditions

Treatment concentration
MGCD0103 concentration-response; shared methods specify 0.1–100 µM drugs. Am80: 0 or 25 µM.
Exposure duration
72 h
Method
Cell-based growth-inhibition assay; shared Methods specify WST-8 Cell Counting Kit-8 with absorbance at 450 nm.
Vehicle
DMSO; final concentration 0.1% or less according to Chemicals.
Co-treatment
MGCD0103 alone versus MGCD0103 with 25 µM Am80.
Reported limits
Table S2 does not provide replicate count, uncertainty or a statistical comparison for these IC50 estimates. Exact MGCD0103 dilution series is not listed. Salt and lot are not specified.
Methods and source locations

Compound reported in the paper: MGCD0103 (mocetinostat); Compound label in the paper: MGCD0103; Adooq Bioscience; salt unspecified

Reported MGCD0103 experiment; no lot validation or demonstrated free-base equivalence.

Supplementary Table S2, printed S4 / PDF page 5; main text Profile of HDAC Isotype Selectivity and Methods: Chemicals / Measurement of Growth-Inhibitory Potency

LNCaP growth inhibition without Am80: 72 h cell-based concentration-response; this is an endpoint, not a fixed treatment dose. — Supplementary Table S2, printed S4 / PDF page 5; main text Profile of HDAC Isotype Selectivity and Methods: Chemicals / Measurement of Growth-Inhibitory Potency

LNCaP growth inhibition in the presence of 25 µM Am80: 72 h cell-based concentration-response in combination with Am80. — Supplementary Table S2, printed S4 / PDF page 5; main text Profile of HDAC Isotype Selectivity and Methods: Chemicals / Measurement of Growth-Inhibitory Potency

Gli1 K518R limits the antiproliferative response to mocetinostat in DAOY cells

Cell-based study · Human DAOY medulloblastoma cells stably expressing wild-type Gli1 or non-acetylatable Gli1 K518R [1]

At 0.5 µM, mocetinostat reduced cell accumulation in wild-type Gli1-expressing DAOY cells, while K518R-expressing cells did not show a significant treatment-associated reduction. The mutant also had higher baseline proliferation. This supports involvement of Gli1 K518 acetylation in this model; it is not a purified-enzyme selectivity measurement.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Cell accumulation with wild-type Gli1 versus Gli1 K518RQualitative response and reported significance WT: lower cell counts at 24 and 48 h (**P < 0.01); K518R: NS at both time points. n = 3; cells seeded in triplicate.[1]

Literature-Reported Treatment Conditions

Treatment concentration
0.5 µM MGCD0103
Exposure duration
24 and 48 h; baseline also shown
Method
Cell counting in the Gli1 construct-by-treatment comparison.
Vehicle
DMSO control; final DMSO concentration not specified in the selected methods.
Reported limits
Exact numerical cell counts are not tabulated and were not estimated from bars. Final DMSO concentration is not specified.
Methods and source locations

Compound reported in the paper: MGCD0103 (mocetinostat); Compound label in the paper: In-house synthesized mocetinostat dihydrobromide salt

Dihydrobromide experiment only; reported concentration retained without salt conversion or Adooq equivalence.

Figure 3g; Results: The effect of Mocetinostat on Hh-regulated functions is dependent on Gli1 acetylation; Methods: Drugs / Cell proliferation and BrdU incorporation assays / Statistical analysis; Supplementary Figure S2c and legend

Cell accumulation with wild-type Gli1 versus Gli1 K518R: Direct cell counts; Figure 3g. General Statistics: mean ± SD, Mann–Whitney U test. n = 3 is the caption designation, not nine independent experiments. — Figure 3g; Results: The effect of Mocetinostat on Hh-regulated functions is dependent on Gli1 acetylation; Methods: Drugs / Cell proliferation and BrdU incorporation assays / Statistical analysis; Supplementary Figure S2c and legend

In Vivo Studies

In nude mice bearing subcutaneous SHH medulloblastoma allografts, daily oral MGCD0103 at 170 mg/kg reduced tumor growth relative to water control during a 20-day observation period (n = 8 per group). The study tested in-house mocetinostat dihydrobromide; this reported dose does not establish an equivalent dose for the catalog free base. [1]

Oral mocetinostat suppressed growth of SHH medulloblastoma allografts

Animal study · Athymic nude mice with subcutaneous primary SHH medulloblastoma allografts [1]

Daily oral treatment with 170 mg/kg MGCD0103 dihydrobromide produced lower tumor volumes than water control over the displayed 20-day experiment (n = 8 per group). This is a subcutaneous tumor experiment, not a blood–brain barrier measurement or a clinical efficacy result.

Measured endpoints — not treatment concentrations
EndpointReported resultReference
Subcutaneous SHH-MB allograft tumor volumeTumor growth versus control Lower than water control at days 10, 15 and 20; n = 8 per group. *P < 0.05 at day 10; **P < 0.01 at days 15 and 20.[1]

Conditions shared by the study groups

Route
Oral (per os)
Frequency
Daily
Treatment course
20-day tumor-volume observation; treatment began when tumors reached approximately 100 mm³.
Vehicle
Water (H2O) comparator stated in Figure 4a caption; active formulation details not further specified.
Study groups and reported outcomes
Group / doseComparatorObserved resultReference
Daily oral mocetinostat dihydrobromide
170 mg/kg MGCD0103; tested material was dihydrobromide salt		H2O per os; n = 8Tumor volumes were lower than control at days 10, 15 and 20; Figure 4a marks *P < 0.05 at day 10 and **P < 0.01 at days 15 and 20.[1]
Daily oral mocetinostat dihydrobromide
Model: Athymic nude mice carrying subcutaneous primary SHH medulloblastoma allografts derived from Math1-Cre/Ptc fl/fl mice; n = 8 per group.
Reported limits: No exact tumor-volume values extracted from the graph. Sex and age of graft recipients and detailed oral formulation are not specified in the selected methods/caption.
Methods and source locations

Compound reported in the paper: MGCD0103 (mocetinostat); Compound label in the paper: In-house synthesized mocetinostat dihydrobromide salt

Reported salt dose in this allograft model only; no salt conversion, free-base exposure equivalence, brain penetration or human treatment recommendation.

Figure 4a–b and caption; Results: MGCD0103 displays strong anticancer effect on mouse models of SHH-MB; Methods: Drugs / In vivo studies / Statistical analysis

Subcutaneous SHH-MB allograft tumor volume: Serial caliper measurements; V = (L × W²)/2. General Statistics: mean ± SD and Mann–Whitney U test. Exact curve values not inferred. — Figure 4a–b and caption; Results: MGCD0103 displays strong anticancer effect on mouse models of SHH-MB; Methods: Drugs / In vivo studies / Statistical analysis

Daily oral mocetinostat dihydrobromide · Figure 4a–b and caption; Results: MGCD0103 displays strong anticancer effect on mouse models of SHH-MB; Methods: Drugs / In vivo studies / Statistical analysis

Specifications

Manufacturer Adooq Bioscience
Actions Inhibitor
CAS Number 726169-73-9
Applications HDAC Inhibitor
Formula C23H20N6O
Molecular Weight 396.4
Synonyms MGCD0103
SMILES
C1=CC=C(C(=C1)N)NC(=O)C2=CC=C(C=C2)CNC3=NC=CC(=N3)C4=CN=CC=C4

Storage & Solubility

In Vitro Solubility

Reported Solubility

SolventReported Solubility
DMSO 12 mg/mL (30.27 mM)
Water Insoluble
Ethanol Insoluble

Preparing Stock Solutions

Stock preparation is unavailable for this product molecular weight.

Calculated stock concentrations do not establish solvent solubility. Refer to the reported solubility data for experimental guidance.

In Vivo Preparation

Concentration
28 mg/mL
Vehicle
30% PEG400+0.5% Tween80+5% Propylene glycol

Storage

Store powder at -20°C, keep desiccated.
In powder form, the chemical is stable for 36 months.
In solution, store at -20°C and use within 1 month to prevent loss of potency. Aliquot to avoid multiple freeze/thaw cycles.

Research References

  1. [1] Coni S, Mancuso AB, Di Magno L, et al. Selective targeting of HDAC1/2 elicits anticancer effects through Gli1 acetylation in preclinical models of SHH Medulloblastoma. Scientific reports (2017). PMID: 28276480 DOI: 10.1038/srep44079 Source material
  2. [2] Ishigami-Yuasa M, Ekimoto H, Kagechika H. Class IIb HDAC Inhibition Enhances the Inhibitory Effect of Am80, a Synthetic Retinoid, in Prostate Cancer. Biological & pharmaceutical bulletin (2019). PMID: 30828077 DOI: 10.1248/bpb.b18-00782 Source material

Publications

2 publications citing this product

  1. Mari Ishigami-Yuasa, .et al. , Biol Pharm Bull, 2019, 42, 448-452 PMID: 30828077
  2. Guang Bai, .et al. , Epigenetics of Chronic Pain, 2019, Pages 1-48

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