2. Cell Cycle/DNA Damage Epigenetics Apoptosis Others
  3. HDAC Apoptosis Drug Intermediate
  4. OKI-005

OKI-005 is an orally active inhibitor of Class I HDACs, with primary targeting of HDAC1, HDAC2 and HDAC3. OKI-005 is a prodrug of OKI-006 (HY-144893). OKI-005 increases histone acetylation levels, induces apoptosis and inhibits cancer cell proliferation. OKI-005 can be used in research related to triple-negative breast cancer and colorectal cancer.

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OKI-005

OKI-005 Chemical Structure

CAS No. : 1351479-95-2

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OKI-005 Related Antibodies

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Description

OKI-005 is an orally active inhibitor of Class I HDACs, with primary targeting of HDAC1, HDAC2 and HDAC3. OKI-005 is a prodrug of OKI-006 (HY-144893). OKI-005 increases histone acetylation levels, induces apoptosis and inhibits cancer cell proliferation. OKI-005 can be used in research related to triple-negative breast cancer and colorectal cancer[1][2].

In Vitro

OKI-005 (0-5 μM; 72 h) potently inhibits the proliferation of most human triple-negative breast cancer (TNBC) and colorectal cancer (CRC) cell lines in vitro, with IC50 values of < 500 nM for most cell lines and IC50 values of < 100 nM for the most sensitive cell lines[1].
OKI-005 (0-500 nM; 24-48 h) induces concentration-dependent apoptosis (measured via caspase-3/7 activity) in sensitive human triple-negative breast cancer (TNBC) cell lines CAL-120 and MDA-MB-231, with activity increased by up to 9-fold, while exerting minimal effects on drug-resistant cell lines HCC1395 and Hs578T[1].
OKI-005 (0-200 nM; 24 h) alters the cell cycle distribution of human triple-negative breast cancer (TNBC) cell lines CAL-120 and MDA-MB-231, increasing the proportion of G1-phase cells and decreasing the proportion of S-phase cells after 24 h of incubation[1].
OKI-005 (0-500 nM; 24 h) induces concentration-dependent increases in acetylated histone H3 and p21 (class I HDAC inhibition markers) in both sensitive and drug-resistant human triple-negative breast cancer (TNBC) cell lines, with only a slight increase in acetylated α-tubulin observed at the highest tested concentration (500 nM)[1].
Combination treatment with OKI-005 (0.1-0.4 μM; 72 h) and Doxorubicin (HY-15142A) exerts synergistic antiproliferative activity in the triple-negative breast cancer (TNBC) cell lines CAL-51, MDA-MB-231, Hs 578T and CAL-120, and this effect is independent of p53 status[2].

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

OKI-005 Related Antibodies

Apoptosis Analysis[1]

Cell Line: Human TNBC cell lines CAL-120, MDA-MB-231, HCC1395, Hs578T
Concentration: 0, 7.8, 15.6, 31.3, 62.5, 125, 250 and 500 nM
Incubation Time: 24 h; 48 h
Result: Induced a concentration-dependent increase in caspase-3/7 activity in sensitive TNBC cell lines CAL-120 and MDA-MB-231, with up to a 7-9-fold increase compared to untreated controls.
Caused minimal increase in apoptosis in resistant TNBC cell lines HCC1395 and Hs578T.

Cell Cycle Analysis[1]

Cell Line: Human TNBC cell lines CAL-120 and MDA-MB-231
Concentration: 0, 25, 100 and 200 nM
Incubation Time: 24 h
Result: Resulted in a trend toward an increase in the G1 cell fraction and a decrease in the S phase cell fraction in CAL-120 cells.
Caused a statistically significant shift to G1 and reduction in S phase in MDA-MB-231 cells.

Western Blot Analysis[1]

Cell Line: Human TNBC cell lines (sensitive and resistant lines, including CAL-120, MDA-MB-231, HCC1395, Hs578T)
Concentration: 0 nM, 50 nM, 200 nM, 500 nM
Incubation Time: 24 h
Result: Induced a concentration-dependent increase in acetylated histone H3 and p21 expression in both sensitive and resistant TNBC cell lines, consistent with class I HDAC inhibition.
Caused a small increase in acetylated α-tubulin at the highest dose (500 nM), potentially indicating weak class IIb HDAC inhibition.
In Vivo

OKI-005 (5-100 mg/kg; p.o., i.p.; daily; 14 days) induces statistically significant, dose-dependent colorectal tumor growth inhibition in BALB/c nude mice, with a maximum TGI of 75.6% at 100 mg/kg p.o., and demonstrates on-target class I HDAC inhibition via increased histone acetylation[1].
OKI-005 (10 mg/kg; i.p.; three times per week; 30 days) statistically significantly inhibits primary triple-negative breast tumor growth and metastasis in BALB/c mice[1].

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

Animal Model: BALB/c nude (male, 6-8 weeks old)[1]
Dosage: 5 mg/kg; 10 mg/kg; 30 mg/kg; 100 mg/kg
Administration: p.o.; daily; 14 days; i.p.; daily; 14 days
Result: Achieved statistically significant tumor growth inhibition of 28.1% at 30 mg/kg p.o. compared to vehicle control.
Achieved statistically significant tumor growth inhibition of 75.6% at 100 mg/kg p.o. compared to vehicle control.
Induced dose-dependent increase in acetyl-histone H3 and acetyl H3K9 at 1 hour post-dose.
Exerted time-dependent increase in acetyl-histone H3 and acetyl H3K9 at 100 mg/kg p.o., with highest levels at 4 hours post-treatment and return to baseline by 24 hours.
Caused weight loss requiring dose reduction in mice treated with 100 mg/kg p.o. at ~1 week.
Animal Model: BALB/c[1]
Dosage: 10 mg/kg
Administration: i.p.; three times per week; 30 days
Result: Statistically significantly inhibited primary tumor growth compared to vehicle control.
Reduced the number of observed thoracic metastases compared to vehicle control.
Molecular Weight

608.81

Formula

C29H44N4O6S2
CAS No.
SMILES

O=C1C2=CSC(CNC(C[C@H](OC([C@@H](NC(C(C)(N1)C)=O)C(C)C)=O)/C=C/CCSC(CCCCCCC)=O)=O)=N2
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Room temperature in continental US; may vary elsewhere.
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Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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OKI-005 Related Classifications

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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:

OKI-0051351479-95-2OKI005OKI 005HDACApoptosisDrug IntermediateHistone deacetylasesDrug Iintermediatecell proliferationcyclin B1BIMG1 phase cell cycle arresthistone deacetylasecolorectal cancerBCL-XLsenescenceapoptosistriple-negative breast cancer cellsInhibitorinhibitorinhibit

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