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Apicidin

Chemicals & Biochemicals

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Article No

AG-CN2-0087-M005

Size

5 mg

Shipping Information

Article No

AG-CN2-0087-M005

Size

5 mg

Specifications

CAS No	183506-66-3
MW	623.8
Article No	AG-CN2-0087-M005
Country Availability	SE, FI, DK, NO, IS, EE, LV, LT
Description	Apicidin
Supplier	Adipogen Life Sciences
Format	Powder
Notes	Antiprotozoal [1]. Potent inhibitor of histone deacetylase (HDAC) [1,2]. Inhibits proliferation [2,3]. Induces cell cycle arrest at the G1 phase [2]. Induces hyperacetylation of histone H4 [5]. Apoptosis inducer [4,8,9]. Potent anti-angiogenic compound [5-7]. Decreases HIF-1alpha protein levels and transcriptional activity in human and mouse tumor cell lines [3]. Autophagy inducer in oral squamous cell carcinoma (OSCC) cells [8]. Promotes either self-renewal or differentiation of embryonic stem cells [10].\|Chemical. CAS: 183506-66-3. Formula: C34H49N5O6. MW: 623.8. Isolated from fungus Fusarium sp. Antiprotozoal. Potent inhibitor of histone deacetylase (HDAC). Inhibits proliferation. Induces cell cycle arrest at the G1 phase. Induces hyperacetylation of histone H4. Apoptosis inducer. Potent anti-angiogenic compound. Decreases HIF-1alpha protein levels and transcriptional activity in human and mouse tumor cell lines. Autophagy inducer in oral squamous cell carcinoma (OSCC) cells. Promotes either self-renewal or differentiation of embryonic stem cells.
Molecular Formula	C34H49N5O6
Alias Names	cyclo-[L-(2-Amino-8-oxodecanoyl)-L-(N-methoxy-tryptophan)-L-isoleucyl-D-pipecolinyl]; OSI-2040
Product Type	Chemicals & Biochemicals
Purity	>98%
Research area	Cell Death
Shipping Information	RT
Size	5 mg
Solubility	Soluble in ethanol or DMSO.
Stability	Stable for at least 1 year after receipt when stored at -20°C. Stock solutions are stable for at least 3 months when stored at -20°C.
Storage	-20°C, 4°C
Technical Specifications	Chemical. CAS: 183506-66-3. Formula: C34H49N5O6. MW: 623.8. Isolated from fungus Fusarium sp. Antiprotozoal. Potent inhibitor of histone deacetylase (HDAC). Inhibits proliferation. Induces cell cycle arrest at the G1 phase. Induces hyperacetylation of histone H4. Apoptosis inducer. Potent anti-angiogenic compound. Decreases HIF-1alpha protein levels and transcriptional activity in human and mouse tumor cell lines. Autophagy inducer in oral squamous cell carcinoma (OSCC) cells. Promotes either self-renewal or differentiation of embryonic stem cells.
Product Page Updated	2024-02-01T08:25:01.492Z

Documentation

Datasheet

MSDS

References

Apicidin: a novel antiprotozoal agent that inhibits parasite histone deacetylase: S.J. Darkin-Rattray, et al.; PNAS 93, 13143 (1996) | Apicidin, a histone deacetylase inhibitor, inhibits proliferation of tumor cells via induction of p21WAF1/Cip1 and gelsolin: J.W. Han, et al.; Cancer Res. 60, 6068 (2000) | Transcriptional activation of p21(WAF1/CIP1) by apicidin, a novel histone deacetylase inhibitor: J.S. Kim, et al.; BBRC 281, 866 (2001) | Apicidin, a histone deacetylase inhibitor, induces apoptosis and Fas/Fas ligand expression in human acute promyelocytic leukemia cells: S.H. Kwon, et al.; J. Biol. Chem. 277, 2073 (2002) | Apicidin, a histone deacetylase inhibitor, induces differentiation of HL-60 cells: J. Hong, et al.; Cancer Lett. 189, 197 (2003) | Regulation of the HIF-1alpha stability by histone deacetylases: S.H. Kim, et al.; Oncol. Rep. 17, 647 (2007) | Apicidin, a novel histone deacetylase inhibitor, has profound anti-growth activity in human endometrial and ovarian cancer cells: T. Ueda, et al.; Int. J. Mol. Med. 19, 301 (2007) | Apicidin, a histone deaceylase inhibitor, induces both apoptosis and autophagy in human oral squamous carcinoma cells: M.Y. Ahn, et al.; Oral. Oncol. 47, 1032 (2011) | Apicidin induces endoplasmic reticulum stress- and mitochondrial dysfunction-associated apoptosis via phospholipase Cgamma1- and Ca(2+)-dependent pathway in mouse Neuro-2a neuroblastoma cells: J.H. Choi, et al.; Apoptosis 17, 1340 (2012) | Histone Deacetylase Inhibitors in Cell Pluripotency, Differentiation, and Reprogramming: A. Kretsovali, et al.; Stem Cells Int. 2012, 1 (2012)

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