Which HDAC isoforms does vorinostat inhibit?

Vorinostat is a pan-inhibitor of zinc-dependent HDACs. It inhibits class I enzymes HDAC1, HDAC2, HDAC3 and HDAC8 and class II enzymes HDAC6 and HDAC10 at nanomolar potency, with reported IC50 values below 86 nM in enzymatic assays. It does not inhibit the NAD+-dependent class III sirtuins. This broad isoform coverage makes it the standard comparator for isoform-selective inhibitors such as the HDAC6-selective agent ricolinostat and the class I selective agent entinostat.

What downstream effects follow HDAC inhibition by vorinostat?

Histone hyperacetylation neutralises the positive charge of lysine residues, loosening histone-DNA contacts and relaxing chromatin. This permits re-expression of epigenetically silenced genes, most prominently the cyclin-dependent kinase inhibitor p21WAF1/CIP1, producing G1 cell-cycle arrest. Vorinostat also acetylates non-histone substrates including p53, alpha-tubulin, HSP90 and NF-kB, leading to HSP90 client protein degradation, disrupted microtubule dynamics, intrinsic and extrinsic apoptosis, autophagy, reactive oxygen species accumulation, and inhibition of angiogenesis.

How should vorinostat be dissolved for cell-based assays?

Vorinostat is soluble in DMSO at 15 mg/mL or greater and also dissolves in ethanol and dimethylformamide, but it is poorly soluble in aqueous buffers. Prepare a 10 to 50 mM DMSO stock, aliquot to avoid freeze-thaw cycles and store at -20 C protected from light and heat; DMSO or ethanol solutions are typically stable for up to six months at -20 C. Dilute into medium keeping the final DMSO concentration at or below 0.1 percent. Typical cellular working concentrations are 0.5 to 10 micromolar for 12 to 48 hours.

Is vorinostat used outside oncology?

Yes. Vorinostat is widely studied as a latency-reversing agent in HIV cure research, where HDAC inhibition reactivates transcription from the latent proviral reservoir in the shock-and-kill strategy. It is also investigated in neurodegeneration, where HDAC inhibition is neuroprotective in Huntington disease and spinal muscular atrophy models, in memory and synaptic plasticity research, in fibrosis, in inflammatory and autoimmune disease models, and in sickle cell and thalassaemia studies of fetal haemoglobin induction.

Is a Certificate of Analysis provided with research-grade vorinostat?

Yes. Every batch ships with a Certificate of Analysis reporting HPLC purity of at least 98 percent, NMR structural confirmation, mass spectrometry, melting point, loss on drying and appearance. MSDS/SDS, residual solvent data and Certificates of Origin are available on request. Vorinostat is classified as a reproductive toxicant and suspected mutagen, so the SDS must be reviewed before handling.

What pack sizes of vorinostat are available?

Research packs of 1 g, 5 g, 10 g and 100 g are held in stock, and 1 KG industrial quantities are supplied made-to-order for process development, formulation work and CMO supply. Bulk quantities qualify for tiered pricing - contact Nutrabiotech Chem with your target quantity and specification for a quotation.

Vorinostat (SAHA) CAS 149647-78-9 | Pan-HDAC Inhibitor, Zolinza, Cancer Epigenetics Research

Vorinostat (SAHA) CAS 149647-78-9
First-in-Class Pan-HDAC Inhibitor

Name: Vorinostat (SAHA)
Brand: Nutrabiotech Chem
SKU: VORI-14964
Price: Inquiry USD
Availability: InStock

Suberoylanilide hydroxamic acid — the first histone deacetylase inhibitor ever approved by the FDA (Zolinza®, 2006) for cutaneous T-cell lymphoma. Its hydroxamic acid warhead chelates the catalytic zinc ion of class I and class II HDACs at nanomolar potency (IC₅₀ < 86 nM), driving histone hyperacetylation, chromatin relaxation, re-expression of silenced tumour suppressor genes, cell-cycle arrest and apoptosis. The definitive reference compound for cancer epigenetics, chromatin biology, autophagy, differentiation therapy and HIV latency-reversal research.

Pan-HDAC Inhibitor Class I & Class II HDAC Cancer Epigenetics CTCL / Zolinza® Histone Hyperacetylation Apoptosis & Autophagy Inducer Latency Reversal Agent

Request a Quote Technical Specs

264.32

MW (C14H20N2O3)

≥98%

Purity (HPLC)

<86 nM

HDAC IC₅₀

Molecular Information

Name: Vorinostat (SAHA)
CAS: 149647-78-9
Formula: C14H20N2O3
MW: 264.32 g/mol
Purity: ≥98% (HPLC)
Solubility: DMSO (≥15 mg/mL),
ethanol, DMF
SMILES: ONC(=O)CCCCCCC(=O)
Nc1ccccc1
InChIKey: WAEXFXRVDQXREF
-UHFFFAOYSA-N
MP: 161-162°C
Appearance: White to off-white powder
Synonyms: SAHA / Zolinza / MK-0683 /
Suberanilohydroxamic acid
Storage: -20°C, sealed, protect from light

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CAS Number

149647-78-9

⚖️

Molecular Weight

264.32

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Primary Activity

Pan-HDAC Inhibitor

✅

Purity

≥98%

Vorinostat (SAHA) Technical Specifications & Quality Control Data

Complete physicochemical properties, structural identifiers and QC release parameters for research-grade Vorinostat (CAS 149647-78-9)

📋 Physicochemical Properties

Product NameVorinostat (SAHA)
IUPAC NameN-Hydroxy-N'-phenyloctanediamide
CAS Number149647-78-9
Development CodeMK-0683
Brand NameZolinza®
Molecular FormulaC14H20N2O3
Molecular Weight264.32 g/mol
Exact Mass264.1474 Da
SMILESONC(=O)CCCCCCC(=O)Nc1ccccc1
InChIKeyWAEXFXRVDQXREF-UHFFFAOYSA-N
AppearanceWhite to off-white / tan powder
Melting Point161-162°C
Density~1.2 g/cm³
pKa (predicted)9.48 ± 0.20
LogP~0.86
MDL NumberMFCD00945317
PubChem CID5311
ATC CodeL01XH01

🔬 Quality Control & Handling

Purity (HPLC)≥98%
Identity1H-NMR / 13C-NMR / LC-MS conform
FormCrystalline powder
ColorWhite to tan
Loss on Drying≤0.5%
Residue on Ignition≤0.1%
Heavy Metals≤20 ppm
Storage Condition-20°C, sealed, dry; heat sensitive
Solution StabilityDMSO or ethanol, -20°C, up to 6 months
SolubilityDMSO ≥15 mg/mL; ethanol; DMF; poorly soluble in water
GHS ClassificationDanger; Muta. 2 (H341); Repr. 1A (H360); handle with containment
QC DocumentationCOA / HPLC / NMR / MS / MSDS
Pack Sizes1g / 5g / 10g / 100g / 1KG
Stock StatusIn Stock
Use StatementResearch use only; not for human or clinical use

HDAC Isoform Coverage & Downstream Substrate Network

Vorinostat inhibits the zinc-dependent HDAC superfamily broadly, and the resulting hyperacetylation extends far beyond histones into a wide non-histone substrate landscape

🧬 HDAC1 (Class I) 🧬 HDAC2 (Class I) 🧬 HDAC3 (Class I) 🧬 HDAC8 (Class I) 🧩 HDAC6 (Class IIb, Tubulin) 🧩 HDAC10 (Class IIb) ⚛️ Catalytic Zn²⁺ Coordination Site 📜 Histone H3 / H4 Acetylation 🔐 p21^WAF1/CIP1 Re-expression 🦠 p53 Acetylation 🪨 α-Tubulin Acetylation (HDAC6) 🎯 HSP90 Acetylation & Client Degradation 🔥 NF-κB / STAT Signalling ♻️ Autophagy & ROS Induction 🩸 Angiogenesis (HIF-1α / VEGF)

How Vorinostat Works: HDAC Inhibition & Epigenetic Reprogramming

From zinc chelation in the enzyme active site to chromatin decompaction and tumour cell death — the mechanistic cascade of pan-HDAC inhibition

Three-Part Pharmacophore Docking

Vorinostat's linear seven-carbon aliphatic linker threads down the narrow hydrophobic channel of the HDAC catalytic pocket, while the terminal anilide "cap" group engages the rim residues at the channel entrance, positioning the warhead precisely.

Catalytic Zinc Chelation

The hydroxamic acid moiety bidentately coordinates the Zn²⁺ ion at the base of the active site, displacing the water molecule required for amide hydrolysis. This blocks deacetylation of acetyl-lysine substrates at nanomolar concentrations (IC₅₀ < 86 nM).

Histone Hyperacetylation

With HDAC activity suppressed, histone acetyltransferase activity dominates and acetyl marks accumulate on H3 and H4 lysine residues, neutralising their positive charge and weakening the electrostatic grip of histones on DNA.

Chromatin Relaxation & Gene Re-expression

Nucleosomes decompact into transcriptionally permissive euchromatin, allowing RNA polymerase II access to epigenetically silenced promoters. The cyclin-dependent kinase inhibitor p21^WAF1/CIP1 is the canonical re-activated tumour suppressor.

Non-Histone Substrate Acetylation

Acetylation of p53 stabilises and activates it; acetylation of HSP90 abolishes chaperone function and triggers degradation of oncogenic client proteins (BCR-ABL, HER2, AKT); HDAC6 inhibition hyperacetylates α-tubulin and disrupts aggresome-mediated protein clearance.

Cell-Cycle Arrest, Apoptosis & Autophagy

The integrated response is G1 (and G2/M) arrest, intrinsic and extrinsic apoptosis via BAX/BAK and death receptor upregulation, reactive oxygen species accumulation, autophagic flux, terminal differentiation and inhibition of tumour angiogenesis.

Vorinostat (SAHA) Research Applications & Disease Models

As the most extensively published HDAC inhibitor, vorinostat underpins work across oncology, epigenetics, virology, neuroscience and immunology

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HDAC Biology & Cancer Epigenetics

The universal reference pan-HDAC inhibitor for chromatin immunoprecipitation, ATAC-seq, acetyl-histone Western blotting, HDAC enzymatic assays and epigenome-wide profiling. Serves as the benchmark against which isoform-selective agents such as entinostat (class I) and ricolinostat (HDAC6) are compared.

Reference Inhibitor

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Cutaneous T-Cell Lymphoma (CTCL)

The approved indication and the disease in which HDAC inhibition is most effective. Used in mycosis fungoides and Sézary syndrome cell lines (HuT-78, HH, MyLa) and xenografts to probe why malignant T cells display exceptional HDAC-inhibitor sensitivity.

FDA-Approved Indication

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Solid Tumour & Haematologic Malignancy Models

Broadly active in glioblastoma, breast, prostate, lung, ovarian, pancreatic and colorectal cancer models as well as multiple myeloma, AML and lymphoma. Frequently used to establish HDAC dependency and to identify epigenetically silenced driver pathways.

Oncology

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Combination Chemotherapy & Chemosensitisation

Synergises with platinum agents, taxanes, proteasome inhibitors (bortezomib), DNA methyltransferase inhibitors (azacitidine, decitabine), BET inhibitors, PARP inhibitors and radiotherapy. Chromatin relaxation increases DNA accessibility to damaging agents and impairs homologous recombination repair.

Synergy Studies

♻️

Autophagy & Programmed Cell Death

Induces autophagic flux (LC3-I to LC3-II conversion, p62 turnover) alongside caspase-dependent apoptosis, providing a tractable system for dissecting the cytoprotective versus cytotoxic roles of autophagy and for testing autophagy-inhibitor combination strategies such as chloroquine co-treatment.

Cell Death Biology

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Differentiation Therapy & Stem Cell Research

Historically derived from dimethyl sulfoxide-induced erythroleukaemia differentiation studies, vorinostat remains a standard differentiation-inducing agent. Applied in iPSC reprogramming, mesenchymal and neural stem cell differentiation, and fetal haemoglobin induction for sickle cell and thalassaemia research.

Differentiation

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HIV Latency Reversal ("Shock and Kill")

One of the most studied latency-reversing agents. HDAC inhibition at the HIV-1 LTR reactivates transcription from the latent proviral reservoir in resting CD4+ T cells, an essential component of HIV cure strategies evaluated in both J-Lat cell models and clinical proof-of-concept studies.

Virology

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Neuroscience & Neurodegeneration

HDAC inhibition is neuroprotective and pro-cognitive in models of Huntington disease, spinal muscular atrophy, Friedreich ataxia, Alzheimer disease and memory consolidation, where histone acetylation regulates activity-dependent gene programmes and synaptic plasticity.

CNS Research

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Inflammation, Fibrosis & Immunomodulation

Suppresses pro-inflammatory cytokine production via NF-κB and STAT pathways, expands regulatory T cells, and attenuates fibroblast activation in pulmonary, hepatic and cardiac fibrosis models — extending vorinostat's utility well beyond oncology.

Immunology

Key Publications on Vorinostat & HDAC Inhibition

Foundational discovery papers, mechanistic studies and the registration trial that established HDAC inhibitors as a drug class

Richon VM, Emiliani S, Verdin E, et al. A class of hybrid polar inducers of transformed cell differentiation inhibits histone deacetylases. Proceedings of the National Academy of Sciences USA. 1998;95(6):3003-3007. — the paper identifying HDAC as the molecular target of SAHA.

doi: 10.1073/pnas.95.6.3003

Marks PA, Richon VM, Rifkind RA. Histone deacetylase inhibitors: inducers of differentiation or apoptosis of transformed cells. Journal of the National Cancer Institute. 2000;92(15):1210-1216.

doi: 10.1093/jnci/92.15.1210

Olsen EA, Kim YH, Kuzel TM, et al. Phase IIb multicenter trial of vorinostat in patients with persistent, progressive, or treatment refractory cutaneous T-cell lymphoma. Journal of Clinical Oncology. 2007;25(21):3109-3115.

doi: 10.1200/JCO.2006.10.2434

Duvic M, Talpur R, Ni X, et al. Phase 2 trial of oral vorinostat (suberoylanilide hydroxamic acid, SAHA) for refractory cutaneous T-cell lymphoma. Blood. 2007;109(1):31-39.

doi: 10.1182/blood-2006-06-025999

Marks PA, Breslow R. Dimethyl sulfoxide to vorinostat: development of this histone deacetylase inhibitor as an anticancer drug. Nature Biotechnology. 2007;25(1):84-90.

doi: 10.1038/nbt1272

Finnin MS, Donigian JR, Cohen A, et al. Structures of a histone deacetylase homologue bound to the TSA and SAHA inhibitors. Nature. 1999;401(6749):188-193.

doi: 10.1038/43710

Archin NM, Liberty AL, Kashuba AD, et al. Administration of vorinostat disrupts HIV-1 latency in patients on antiretroviral therapy. Nature. 2012;487(7408):482-485.

doi: 10.1038/nature11286

Vorinostat Pack Sizes & Ordering Information

Research-grade Vorinostat / SAHA (CAS 149647-78-9) supplied in 1g / 5g / 10g / 100g / 1KG with full QC documentation; custom bulk quantities supported

Tier	Pack Size	Stock Status	Suitable For	Shipping & Lead Time
Standard	1 g	In Stock	HDAC enzymatic assays, acetyl-histone Western blots, cell viability screens	Ambient shipping with ice pack; same/next-day dispatch
Medium	5 g	In Stock	Rodent xenograft dosing, combination synergy matrices, ChIP-seq programmes	Cold-chain or ambient; same/next-day dispatch
Large	10 g	In Stock	Long-term in vivo studies, multi-lab consortia, compound library restocking	Cold-chain shipping; same/next-day dispatch
Bulk	100 g	In Stock	Formulation and nanoparticle delivery development, toxicology batches, reference standards	Insulated carton with COA; quote to confirm dispatch
Industrial	1 KG	Made to order	Pilot and production scale, CMO/CDMO supply, process validation campaigns	Drum shipment with batch COA; scheduled batch delivery

💡 Reference pack sizes shown above; for exact pricing, lot availability and bulk vorinostat (SAHA) supply please contact us for a quote. Tiered discounts apply to bulk orders.

Frequently Asked Questions (FAQ)

What is Vorinostat (SAHA, CAS 149647-78-9), and why is it important?

Vorinostat, also known as suberoylanilide hydroxamic acid (SAHA), is a synthetic hydroxamic acid (C14H20N2O3, MW 264.32) and the first histone deacetylase (HDAC) inhibitor approved by the FDA, marketed as Zolinza. It is a landmark epigenetic probe because it validated HDAC inhibition as a therapeutic strategy and remains one of the most widely used tools for studying chromatin, acetylation and transcriptional control. It was developed from work at Columbia University and Memorial Sloan-Kettering.

How does Vorinostat inhibit HDAC enzymes?

Vorinostat's terminal hydroxamic acid group (-C(=O)NOH) acts as a zinc-binding warhead. It chelates the catalytic Zn²⁺ ion in the HDAC active site, blocking the hydrolysis of the acetyl-lysine amide bond. By occupying the pocket that normally accommodates the acetyl group, SAHA locks the enzyme in an inactive conformation. This zinc-chelating mechanism is shared by hydroxamate HDAC inhibitors such as trichostatin A and panobinostat.

Which HDAC isoforms does Vorinostat target?

Vorinostat is a pan-HDAC inhibitor with activity against both class I HDACs (HDAC1, HDAC2, HDAC3, HDAC8) and class II HDACs (HDAC6, HDAC10) at nanomolar concentrations. Reported IC50 values are below 86 nM for several isoforms. It has much weaker activity against the NAD⁺-dependent class III sirtuins, making it a useful tool for separating zinc-dependent HDAC function from sirtuin biology.

What downstream cellular effects result from HDAC inhibition by Vorinostat?

Inhibiting HDACs causes histone hyperacetylation, chromatin relaxation and re-expression of silenced tumour-suppressor and differentiation genes. Downstream effects include cell-cycle arrest (via p21/WAF1 induction), apoptosis, autophagy, terminal differentiation and reduced angiogenesis. These pleiotropic effects explain its broad utility across oncology, neuroscience and virology research.

Why is Vorinostat approved for cutaneous T-cell lymphoma (CTCL)?

Vorinostat was approved for CTCL (mycosis fungoides and Sézary syndrome) in patients who have progressed on or relapsed after two systemic therapies. In CTCL, HDAC dysregulation contributes to malignant T-cell survival; vorinostat's ability to drive cell-cycle arrest, apoptosis and differentiation of cutaneous T-cells produced meaningful clinical responses. It remains a reference standard for epigenetic therapy in this indication.

How does Vorinostat compare with Romidepsin and Panobinostat?

Romidepsin is a natural-product, class I-selective HDAC inhibitor (a cyclic depsipeptide) with a different zinc-binding group (a disulfide that reduces to a thiol in cells). Panobinostat is a more potent, broader pan-HDAC inhibitor (also class I/II) used in multiple myeloma. Vorinostat is unique as the first-in-class hydroxamate HDACi and is valued for its balanced class I/II coverage and well-characterised pharmacology, whereas romidepsin is class I-selective and panobinostat is generally more potent and broader.

How should Vorinostat (SAHA) be dissolved for biological assays?

Vorinostat is soluble in DMSO (commonly reported up to ~50 mg/mL for stock solutions) and also dissolves in ethanol. For cell-based work, prepare a concentrated DMSO stock, aliquot and store at -20°C protected from light, then dilute into aqueous media keeping final DMSO ≤0.1% v/v. For in vivo studies, vehicles such as DMSO/PEG/saline mixtures are used. Always confirm solubility and stability for your specific assay.

Is Vorinostat used in research outside of oncology?

Yes. Beyond cancer, SAHA is a key probe in neuroscience (neuronal differentiation, neuroprotection, glioblastoma models), HIV latency reversal (it can reactivate latent provirus in "shock-and-kill" strategies), autophagy and anti-inflammatory research. Its ability to remodel the epigenome makes it broadly applicable wherever acetylation-dependent transcriptional control is studied.

Is a Certificate of Analysis (COA) provided with Vorinostat?

Yes. Every batch of research-grade Vorinostat (CAS 149647-78-9) ships with a Certificate of Analysis including HPLC purity (≥98%), NMR structural confirmation and mass-spectrometry data. MSDS/SDS, solubility datasheets and Certificates of Origin are available on request. Please contact us for documentation.

What pack sizes and stock status are available?

Vorinostat / SAHA is supplied in 1 g, 5 g, 10 g and 100 g pack sizes (all In Stock) and a 1 KG industrial tier (Made to order). Custom bulk quantities and special packaging are supported for CMO/CDMO and process-validation campaigns. For exact pricing and lot availability, request a quote.

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Research-grade Vorinostat / SAHA (CAS 149647-78-9) — purity ≥98%, COA included
The first-in-class pan-HDAC inhibitor for epigenetics, CTCL and chromatin research — request a quote today

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Weight	10 g

Vorinostat CAS 149647-78-9 98% Purity Pan HDAC Inhibitor Powder SAHA