Product Overview

Dimethylcurcumin (ASC-J9, 1,7-Bis(3,4-dimethoxyphenyl)hepta-1,6-diene-3,5-dione, CAS 52328-98-0, C₂₃H₂₄O₆, MW ~396.43 g/mol, synonym GO-Y025) is a synthetic curcuminoid derivative that functions as a selective androgen receptor (AR) degrader — a mechanism distinct from conventional AR antagonists and AR knockdown approaches. ASC-J9 promotes AR protein ubiquitination and proteasome-mediated degradation without altering AR mRNA levels, providing a purely post-translational mechanism of AR suppression. Developed as an optimized curcumin analog, ASC-J9 incorporates a critical 3,4-dimethoxy substitution on both phenyl rings that blocks the Phase II glucuronidation and sulfation metabolic conjugation sites present in natural curcumin. This single structural modification addresses the most significant limitation of curcumin as a research tool — poor systemic bioavailability (plasma t₁/₂ ~0.1–0.2 h for curcumin vs ~1.5–2 h for ASC-J9). Preclinical studies demonstrate ASC-J9 efficacy across multiple AR-driven disease models: castration-resistant prostate cancer (CRPC) including enzalutamide-resistant cell lines, androgenetic alopecia via AR degradation in dermal papilla cells, acne vulgaris through sebocyte AR suppression, and spinal bulbar muscular atrophy (SBMA / Kennedy disease) via mutant polyglutamine-AR aggregate clearance. ASC-J9 shows high receptor selectivity — degrading AR protein without affecting ER, PR, GR, or MR. UPOR Biotech provides dimethylcurcumin (ASC-J9) as a Research Grade (≥98% HPLC) compound with High Purity (≥99% HPLC) available for sensitive applications. Every shipment includes full analytical documentation.

As a leading dimethylcurcumin (ASC-J9) manufacturer and bulk supplier, UPOR Biotech provides high-purity ASC-J9 for academic research institutions, pharmaceutical R&D, biotechnology companies, and contract research organizations (CROs) worldwide. ASC-J9’s unique mechanism — AR degradation without AR mRNA alteration — makes it an essential research tool for AR biology, prostate cancer drug discovery, and androgen-driven disease research. Custom synthesis and bulk packaging available with flexible MOQ starting at 10 mg. Free sample available for qualified B2B buyers and research institutions. Every shipment includes full documentation: COA, MSDS, HPLC chromatogram, ¹H NMR, and mass spectrum.

ASC-J9 vs Natural Curcumin — 10× Half-Life: Why Dimethoxy Substitution Creates the Research-Grade Curcuminoid

Natural curcumin’s Achilles’ heel is its vanishingly short plasma half-life (~0.1–0.2 h) — driven by rapid Phase II conjugation of the free phenolic -OH groups via UGT-glucuronidation and SULT-sulfation. This metabolic vulnerability makes natural curcumin nearly undetectable in plasma after oral administration and severely limits its utility as an in vivo research tool. ASC-J9 solves this through a single, elegant structural modification: replacing the two phenolic -OH groups on each phenyl ring with methoxy (-OCH₃) groups (3,4-dimethoxy substitution). This blocks the primary metabolic conjugation sites, extending plasma half-life approximately 10-fold to ~1.5–2 hours and enabling sustained systemic exposure. Beyond bioavailability, ASC-J9 introduces a completely distinct biological mechanism — selective AR protein degradation via the ubiquitin-proteasome pathway — that natural curcumin does not possess. ASC-J9 binds to AR, promotes AR ubiquitination, and targets AR for proteasome-mediated degradation without affecting AR mRNA transcription or other steroid hormone receptors. This makes ASC-J9 the preferred curcuminoid scaffold for in vivo AR-targeting research across prostate cancer, alopecia, acne, and neurodegenerative disease models. The dimethoxy modification also improves chemical stability, photostability, and cellular membrane permeability compared to natural curcumin.

Technical Specifications

PropertySpecification
Product NameDimethylcurcumin (ASC-J9) — Research Grade (≥98% HPLC)
SynonymsASC-J9; Dimethylcurcumin; 1,7-Bis(3,4-dimethoxyphenyl)hepta-1,6-diene-3,5-dione; GO-Y025; Curcumin analog; 3,4-Dimethoxycurcumin
CAS Number52328-98-0
Molecular FormulaC₂₃H₂₄O₆
Molecular Weight~396.43 g/mol
SourceSynthetic — curcuminoid derivative; 3,4-dimethoxy-substituted curcumin analog
Key Advantage / MechanismSelective androgen receptor (AR) degrader via ubiquitin-proteasome pathway. Promotes AR ubiquitination and proteasome-mediated degradation without affecting AR mRNA levels. 3,4-Dimethoxy substitution blocks Phase II metabolic conjugation (glucuronidation/sulfation), extending plasma half-life ~10× vs natural curcumin.
AppearanceYellow to orange crystalline powder
Assay (Research Grade)≥98.0% (HPLC, area normalization at 254 nm)
Assay (High Purity)≥99.0% (HPLC) available upon request for sensitive applications
IdentificationHPLC retention time matches reference standard; ¹H NMR spectrum conforms to structure; MS (ESI+) m/z 397.2 [M+H]⁺; ¹³C NMR consistent with C₂₃H₂₄O₆
Loss on Drying≤0.5% (60°C, vacuum)
Melting Point~130–134°C (literature)
SolubilitySoluble in DMSO (≥25 mg/mL); soluble in ethanol (~5 mg/mL with warming); soluble in DMF; practically insoluble in water
Heavy Metals (Total)≤10 ppm (as Pb)
Elemental ImpuritiesPb ≤2 ppm; As ≤1 ppm; Hg ≤1 ppm; Cd ≤1 ppm (ICH Q3D compliant)
Microbial LimitsTAMC ≤100 CFU/g; TYMC ≤10 CFU/g (USP <61>); Pathogens (E. coli, Salmonella, S. aureus, P. aeruginosa) — Absent in 10 g (USP <62>)
Residual SolventsICH Q3C Class 3 compliant
Biological Activity (IC₅₀)~5–10 μM in AR-dependent prostate cancer cell lines (LNCaP, C4-2); induces G1 cell cycle arrest and apoptosis
SelectivityDegrades AR protein without affecting ER, PR, GR, or MR. Does not alter AR mRNA levels — purely post-translational mechanism.
Pharmacokinetic AdvantagePlasma half-life ~1.5–2 h vs ~0.1–0.2 h for natural curcumin (~10× improvement). Detectable systemic exposure after oral administration in preclinical models.
Research ApplicationsCastration-resistant prostate cancer (CRPC); androgenetic alopecia; acne vulgaris; spinal bulbar muscular atrophy (Kennedy disease / SBMA); AR-positive breast cancer; AR signaling pathway research
In Vitro StabilityStable in DMSO stock solutions at -20°C for ≥6 months; prepare fresh working solutions for cell-based assays; avoid repeated freeze-thaw cycles
Grade / StandardsResearch Grade (≥98% HPLC); High Purity (≥99% HPLC) available; for laboratory research use only — not for human or veterinary therapeutic use
CertificationsISO 9001:2015; ISO 22000; HACCP; FDA Facility Registration; HALAL; KOSHER; Non-GMO Statement; BSE/TSE-Free Statement
Packaging10 mg / 50 mg / 100 mg / 500 mg / 1 g amber glass vials with PTFE-lined caps under inert atmosphere; bulk packaging available upon request
Storage-20°C, tightly sealed in original amber container, protect from light and moisture; long-term storage recommended at -80°C under argon or nitrogen
Shelf Life2 years from date of manufacture under recommended storage conditions

Key Benefits — Dimethylcurcumin (ASC-J9)

Selective AR Degrader — Ubiquitin-Proteasome Pathway

ASC-J9 promotes androgen receptor (AR) protein degradation via ubiquitination and proteasome-mediated proteolysis — a mechanism distinct from AR antagonists (competitive binding) and AR knockdown (mRNA targeting). AR protein is selectively degraded while AR mRNA transcription remains unchanged, providing a purely post-translational intervention. No cross-reactivity with ER, PR, GR, or MR.

Selective AR Degrader

10× Bioavailability vs Natural Curcumin — Dimethoxy-Stabilized Scaffold

The 3,4-dimethoxy substitution on both phenyl rings blocks Phase II glucuronidation and sulfation — the primary metabolic clearance routes for natural curcumin. Plasma half-life extended from ~0.1–0.2 h (curcumin) to ~1.5–2 h (ASC-J9) — enabling sustained systemic exposure and reliable in vivo pharmacological studies. Improved chemical and photostability.

10× Half-Life

Multi-Indication Research Applications Across AR-Driven Diseases

Validated in preclinical models of castration-resistant prostate cancer (including enzalutamide-resistant cell lines), androgenetic alopecia (hair regrowth), acne vulgaris (sebum reduction), spinal bulbar muscular atrophy (mutant AR aggregate clearance), and AR-positive breast cancer. Multi-indication AR research tool.

Multi-Indication

High Purity — ≥98% HPLC with Full Analytical Documentation

Available in Research Grade (≥98% HPLC) and High Purity (≥99% HPLC). Every shipment includes COA, HPLC chromatogram, ¹H NMR spectrum, mass spectrum, MSDS, and full lot traceability. QC tested for purity, identity, residual solvents (ICH Q3C), heavy metals, and microbial limits. Free sample for qualified buyers.

≥98% HPLC

Applications

Castration-Resistant Prostate Cancer (CRPC) Research

ASC-J9 suppresses AR target genes (PSA, TMPRSS2), induces G1 arrest and apoptosis in LNCaP, C4-2, and 22Rv1 cells — including enzalutamide-resistant models. Reduces tumor xenograft growth in preclinical models. For laboratory research use only.

Androgenetic Alopecia / Hair Loss Research

Topical ASC-J9 promotes hair regrowth in preclinical alopecia models by degrading AR in dermal papilla cells — interrupting the AR → TGF-β1 → catagen signaling cascade. Emerging topical formulation research. For laboratory research use only.

Acne Vulgaris / Sebum Regulation Research

AR degradation in sebocytes reduces sebum production — a mechanism-based approach to acne pathogenesis research. ASC-J9 targets the AR-driven component of sebaceous gland activity without systemic anti-androgen effects. For laboratory research use only.

Spinal Bulbar Muscular Atrophy (Kennedy Disease) Research

ASC-J9 degrades polyglutamine-expanded mutant AR aggregates — key pathological drivers of SBMA. Preclinical studies demonstrate reduced mutant AR aggregation and improved motor function in SBMA models. For laboratory research use only.

AR-Positive Breast Cancer Research

Emerging research demonstrates ASC-J9 efficacy in AR-dependent breast cancer subtypes where AR functions as an oncogenic driver. AR degradation suppresses AR-mediated proliferative signaling. For laboratory research use only.

Curcuminoid Bioavailability & SAR Studies

ASC-J9 as a model compound for structure-activity relationship (SAR) studies of curcuminoid derivatives. The 3,4-dimethoxy scaffold demonstrates how targeted substitution blocks metabolic conjugation — informing next-generation curcuminoid design. For laboratory research use only.

Frequently Asked Questions

Dimethylcurcumin (ASC-J9, CAS 52328-98-0, C₂₃H₂₄O₆, MW ~396.43 g/mol) is a synthetic curcuminoid derivative and selective androgen receptor (AR) degrader. Unlike AR antagonists (enzalutamide, bicalutamide) that competitively block the AR ligand-binding domain, ASC-J9 uses a post-translational mechanism: it binds to AR, promotes AR ubiquitination through enhanced E3 ligase recruitment, and targets AR for proteasome-mediated degradation. This selectively reduces AR protein levels without altering AR mRNA transcription — confirmed by unchanged AR mRNA on qRT-PCR while AR protein drops on Western blot. ASC-J9 does not affect other steroid hormone receptors (ER, PR, GR, MR), demonstrating high receptor selectivity. The 3,4-dimethoxy substitution on both phenyl rings blocks Phase II glucuronidation and sulfation conjugation — the metabolic pathways that rapidly clear natural curcumin (t₁/₂ ~0.1–0.2 h). This extends ASC-J9 plasma half-life to ~1.5–2 h (~10× improvement). UPOR Biotech provides ASC-J9 at ≥98% HPLC (Research Grade) with ≥99% available.

ASC-J9 has demonstrated preclinical efficacy across five AR-driven disease research areas. (1) Castration-resistant prostate cancer (CRPC): ASC-J9 suppresses AR target genes (PSA, TMPRSS2), induces G1 cell cycle arrest and apoptosis in AR-positive prostate cancer cell lines (LNCaP, C4-2, 22Rv1) — including enzalutamide-resistant models — and reduces tumor xenograft growth in mouse models. (2) Androgenetic alopecia: topical ASC-J9 promotes hair regrowth in testosterone-induced alopecia mouse models by degrading AR in dermal papilla cells, which interrupts the AR → TGF-β1 → catagen (hair follicle regression) signaling cascade. (3) Acne vulgaris: AR degradation in sebocytes reduces sebum production — a mechanism-based research approach to acne pathogenesis. (4) Spinal bulbar muscular atrophy (SBMA / Kennedy disease): ASC-J9 degrades polyglutamine-expanded mutant AR aggregates that drive neurodegeneration in this inherited condition — preclinical studies show reduced aggregate burden and improved motor function. (5) AR-positive breast cancer: emerging data suggests efficacy where AR functions as an oncogenic driver. All applications are for laboratory research use only — not for human or veterinary therapeutic use.

The defining advantage of ASC-J9 over natural curcumin is its ~10× extended plasma half-life — achieved through a single critical structural modification. Natural curcumin contains free phenolic hydroxyl (-OH) groups on its phenyl rings that undergo rapid Phase II metabolism — glucuronidation by UGT enzymes and sulfation by SULT enzymes — resulting in extensive first-pass metabolism, a plasma half-life of only ~0.1–0.2 hours, and virtually undetectable systemic levels after oral administration. ASC-J9 replaces these -OH groups with methoxy (-OCH₃) groups (3,4-dimethoxy substitution), effectively blocking the primary metabolic conjugation sites. This extends plasma half-life to ~1.5–2 hours (~10× improvement), maintains detectable systemic concentrations after oral administration in preclinical models, and improves tissue distribution. Beyond bioavailability, ASC-J9 introduces a distinct pharmacological mechanism — selective AR protein degradation via the ubiquitin-proteasome pathway — that natural curcumin does not possess. ASC-J9 also demonstrates improved chemical stability, photostability, and cellular membrane permeability versus natural curcumin. For in vivo AR-targeting research, ASC-J9 is the preferred curcuminoid scaffold because it provides both the bioavailability and the mechanism that natural curcumin lacks.

UPOR Biotech provides Dimethylcurcumin (ASC-J9) in two purity grades to match research requirements. Research Grade (≥98% HPLC) — the standard grade suitable for routine in vitro assays (cell viability, Western blot, qRT-PCR, reporter gene assays), biochemical studies (AR binding, ubiquitination assays), and preclinical in vivo models. This is the most commonly ordered grade. High Purity Grade (≥99% HPLC) — recommended for sensitive quantitative applications including dose-response pharmacology studies, reference standard preparation, publication-quality research, and any application where maximum purity confidence is required. Both grades are supplied with full analytical documentation: Certificate of Analysis (COA) with HPLC purity, retention time, and full impurity profile; signed and dated HPLC chromatogram; ¹H NMR spectrum; mass spectrum (ESI+); MSDS; and lot-specific quality data. Each batch undergoes rigorous QC including HPLC purity analysis (area normalization, 254 nm), identity confirmation (NMR, MS), residual solvent testing per ICH Q3C, heavy metals analysis (Pb, As, Hg, Cd), and microbial limits testing per USP <61>/<62>. Packaging: 10 mg to 1 g amber glass vials with PTFE-lined caps. MOQ: 10 mg. Free sample available for qualified research institutions.

Every shipment of Dimethylcurcumin (ASC-J9) includes a comprehensive documentation package: Certificate of Analysis (COA) with HPLC purity (≥98% or ≥99%), retention time, full impurity profile, heavy metals (≤10 ppm total; Pb ≤2 ppm, As ≤1 ppm, Hg ≤1 ppm, Cd ≤1 ppm), residual solvents per ICH Q3C, and microbial limits per USP <61>/<62>; Material Safety Data Sheet (MSDS); Signed and dated HPLC Chromatogram; ¹H NMR Spectrum confirming structural identity; Mass Spectrum (ESI+); BSE/TSE-Free Statement; Non-GMO Statement; Allergen Statement; HALAL Certificate; KOSHER Certificate; ISO 22000 + HACCP; ISO 9001:2015; FDA Facility Registration; Stability Data (-20°C real-time 24-month and accelerated 40°C/75%RH 6-month); and Complete Lot Traceability from raw material to finished product. All documents provided in English. Free sample available for qualified B2B buyers and research institutions. MOQ: 10 mg.