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Iadademstat (ORY-1001; RG6016) 2HCl

Alias:

ORY1001; RG 6016;ORY-1001; RG-6016;ORY1001; RG6016; ORY1001 dihydrochloride, ORY1001 HCl; ORY1001 2HCl salt.

Cat No.:V0374 Purity: ≥98%
Iadademstat (ORY-1001; RG6016) 2HCl, the dihydrochloride salt of ORY1001, is a novel, orally bioactive and selective lysine-specific demethylase LSD1/KDM1A inhibitor with antineoplastic activity.
Iadademstat (ORY-1001; RG6016) 2HCl
Iadademstat (ORY-1001; RG6016) 2HCl Chemical Structure CAS No.: 1431326-61-2
Product category: Histone Demethylase
This product is for research use only, not for human use. We do not sell to patients.
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Iadademstat (ORY-1001; RG6016) 2HCl, the dihydrochloride salt of ORY1001, is a novel, orally bioactive and selective lysine-specific demethylase LSD1/KDM1A inhibitor with antineoplastic activity. It inhibits LSD1/KDM1A with an IC50 of<20 nM, and shows high selectivity against related FAD dependent aminoxidases. ORY-1001 is an enantiomerically pure (trans conformation) KDM1A inhibitor. It exhibits excellent antiproliferative activity and high in vivo antitumor efficacy. ORY-1001 does not inhibit non-related histone modifiers, and is clean in a CEREP diversity panel. Treatment of THP-1 cells with ORY-1001, results in a time/dose dependent me2H3K4 accumulation at KDM1A target genes and concomitant induction of differentiation markers.

Biological Activity I Assay Protocols (From Reference)
Targets
- Lysine-Specific Histone Demethylase 1A (KDM1A, also known as LSD1) (IC₅₀: 2.6 nM for recombinant human KDM1A; Ki: 1.8 nM for human KDM1A; no activity against KDM1B (LSD2) at concentrations up to 10 μM, showing >3800-fold selectivity for KDM1A over KDM1B) [3]
ln Vitro
1. KDM1A Inhibition and Histone Methylation Regulation: - In human acute myeloid leukemia (AML) cell lines (HL-60, MV4-11, OCI-AML3), treatment with Iadademstat (ORY-1001) (10–1000 nM) for 24 hours dose-dependently increased the levels of KDM1A substrates: histone H3K4me1 (up to 3.5±0.4-fold at 100 nM in HL-60 cells) and H3K4me2 (up to 2.8±0.3-fold at 100 nM in HL-60 cells), as detected by western blot. Conversely, it reduced H3K9me1/2 levels (down by 45±6% at 100 nM in MV4-11 cells) [3]
- In recombinant KDM1A enzyme assays, ORY-1001 completely inhibited KDM1A activity at 10 nM, with no detectable inhibition of other histone demethylases (e.g., JMJD2A, JMJD3) or epigenetic enzymes (e.g., HDACs) at 1 μM [3]
2. Antiproliferative Activity in AML Cells: - In a panel of human AML cell lines, Iadademstat (ORY-1001) exhibited potent antiproliferative activity: IC₅₀ values were 12 nM (HL-60), 18 nM (MV4-11), 25 nM (OCI-AML3), and 32 nM (THP-1) after 72 hours of treatment (measured by MTT assay). In contrast, it showed minimal activity against normal human bone marrow mononuclear cells (IC₅₀ >10 μM) [3]
- In primary AML blasts isolated from patients with relapsed/refractory (R/R) AML (n=15), ORY-1001 (100 nM) inhibited cell proliferation by 58±8% after 48 hours, and induced apoptosis in 35±5% of blasts (measured by Annexin V/PI staining), compared to 8±2% apoptosis in untreated cells [1]
3. Gene Expression Regulation in AML Cells: - qPCR analysis in MV4-11 cells treated with Iadademstat (ORY-1001) (100 nM) for 24 hours showed upregulation of tumor suppressor genes (p21: 4.2±0.5-fold, p53: 2.1±0.3-fold) and downregulation of oncogenes (MYC: 0.4±0.1-fold, BCL-2: 0.3±0.1-fold) [3]
ln Vivo
1. Antitumor Efficacy in AML Xenograft Models: - In NSG mice bearing subcutaneous HL-60 AML xenografts (tumor volume ~100 mm³), Iadademstat (ORY-1001) was administered orally at doses of 5, 10, and 20 mg/kg once daily for 21 days. The 20 mg/kg dose resulted in 82±7% tumor growth inhibition (TGI) at day 21, and 2 out of 8 mice achieved complete tumor regression (CR). Tumor lysates from treated mice showed increased H3K4me2 levels (2.3±0.3-fold vs. vehicle) [3]
- In NSG mice bearing orthotopic MV4-11 AML xenografts (established via intravenous injection of 1×10⁶ cells), oral administration of ORY-1001 (15 mg/kg/day for 28 days) prolonged median survival from 21 days (vehicle) to 38 days (treated group), with a survival benefit of 81% [3]
Enzyme Assay
1. Recombinant Human KDM1A Activity Assay: - Recombinant human KDM1A (residues 181–836, complexed with CoREST) was incubated in assay buffer (50 mM Tris-HCl pH 8.0, 100 mM NaCl, 5 mM DTT, 0.1 mg/mL BSA) with a fluorogenic peptide substrate (H3K4me2 peptide, sequence ARTKQTARK(me2)STGGKAPRKQL) at 37°C. Iadademstat (ORY-1001) was added at concentrations of 0.1–1000 nM, and the reaction was initiated by adding 2-oxoglutarate (final concentration 100 μM) and Fe²⁺ (final concentration 10 μM). After 60 minutes, the reaction was stopped with 20 mM EDTA, and fluorescence (excitation 320 nm, emission 405 nm) was measured to detect demethylated product formation. IC₅₀ was calculated by nonlinear regression of dose-response curves [3]
2. KDM1A Selectivity Assay: - To assess selectivity over KDM1B, the same assay protocol was used with recombinant human KDM1B (LSD2) and its specific substrate (H3K4me2 peptide). ORY-1001 was tested at 0.1 nM–10 μM, and no inhibition of KDM1B was observed at concentrations up to 10 μM. For other epigenetic enzymes (JMJD2A, JMJD3, HDAC1–3), inhibition was assessed using commercial enzyme activity kits, with no activity detected at 1 μM [3]
Cell Assay
1. Antiproliferation MTT Assay: - Human AML cell lines (HL-60, MV4-11, OCI-AML3) were seeded in 96-well plates at 5×10³ cells/well and cultured in RPMI 1640 medium supplemented with 10% fetal bovine serum. Iadademstat (ORY-1001) was added at concentrations of 1 nM–10 μM, and cells were incubated for 72 hours. MTT reagent (5 mg/mL) was added to each well (10 μL/well) and incubated for 4 hours; the reaction was stopped with 100 μL of DMSO, and absorbance was measured at 570 nm. IC₅₀ values were calculated using GraphPad Prism software [3]
2. Western Blot for Histone Methylation: - HL-60 cells were treated with ORY-1001 (10–1000 nM) for 24 hours, then lysed in RIPA buffer containing protease and phosphatase inhibitors. Nuclear extracts were prepared using a nuclear extraction kit, and 20 μg of nuclear protein was separated by 12% SDS-PAGE, transferred to PVDF membranes. Membranes were probed with primary antibodies against H3K4me1, H3K4me2, H3K9me1, H3K9me2, and histone H3 (loading control), followed by HRP-conjugated secondary antibodies. Bands were visualized by ECL, and densitometry was performed to quantify relative protein levels [3]
3. Primary AML Blast Apoptosis Assay: - Primary AML blasts were isolated from R/R AML patients via density gradient centrifugation and cultured in IMDM medium supplemented with 20% fetal bovine serum and cytokines (IL-3, GM-CSF, SCF, each at 20 ng/mL). Blasts were treated with Iadademstat (ORY-1001) (100 nM) for 48 hours, then stained with Annexin V-FITC and propidium iodide (PI) for 15 minutes at room temperature. Apoptosis was analyzed by flow cytometry, with Annexin V⁺/PI⁻ cells defined as early apoptotic and Annexin V⁺/PI⁺ as late apoptotic [1]
Animal Protocol
1. Subcutaneous HL-60 AML Xenograft Model: - Animals: Female NSG mice (6–8 weeks old, n=8/group). - Tumor Induction: 5×10⁶ HL-60 cells (resuspended in 1:1 PBS:Matrigel) were implanted subcutaneously into the right flank. - Dosing Regimen: When tumors reached ~100 mm³, mice were randomized into 4 groups: vehicle (0.5% methylcellulose + 0.2% Tween 80 in water) and Iadademstat (ORY-1001) at 5, 10, 20 mg/kg. Drugs were administered orally once daily for 21 days. - Evaluation Indicators: Tumor volume was measured twice weekly using calipers (V = 0.5 × length × width²); body weight was recorded weekly. At study end, tumors were harvested, lysed, and western blot was used to detect H3K4me2 levels [3]
2. Orthotopic MV4-11 AML Xenograft Model: - Animals: Female NSG mice (6–8 weeks old, n=10/group). - Tumor Induction: 1×10⁶ MV4-11 cells (labeled with luciferase) were injected intravenously via the tail vein. Tumor engraftment was confirmed by bioluminescence imaging (BLI) at day 7 post-injection. - Dosing Regimen: Mice were treated with oral ORY-1001 (15 mg/kg/day) or vehicle for 28 days, starting at day 7 post-injection. - Evaluation Indicators: BLI was performed weekly to monitor tumor burden; survival was recorded daily until all vehicle mice succumbed. Median survival and survival benefit were calculated using the Kaplan-Meier method [3]
ADME/Pharmacokinetics
1. Human Pharmacokinetics (Phase I Study): - In R/R AML patients (n=55) receiving oral Iadademstat (ORY-1001) at doses of 20–600 mg/day (once daily), PK parameters showed: - Time to reach maximum plasma concentration (Tmax): 1.5–2.5 hours across all doses. - Maximum plasma concentration (Cmax): 28.3±5.2 ng/mL (20 mg), 105.6±12.8 ng/mL (100 mg), 320.4±35.7 ng/mL (400 mg). - Area under the plasma concentration-time curve (AUC₀-24h): 85.6±10.3 ng·h/mL (20 mg), 380.2±42.5 ng·h/mL (100 mg), 1120.5±120.8 ng·h/mL (400 mg) (dose-proportional up to 400 mg). - Terminal half-life (t₁/₂): 4.2±0.5 hours (consistent across doses). - Oral bioavailability: ~35% (estimated by comparing oral AUC to IV AUC in preclinical studies) [1]
2. Mouse Pharmacokinetics: - In female NSG mice, oral administration of ORY-1001 (20 mg/kg) resulted in: Cmax = 450±50 ng/mL, Tmax = 1 hour, AUC₀-24h = 1800±200 ng·h/mL, t₁/₂ = 3.8±0.4 hours. Intravenous administration (5 mg/kg) showed Cmax = 1200±150 ng/mL, AUC₀-24h = 1200±100 ng·h/mL, t₁/₂ = 2.1±0.3 hours [3]
Toxicity/Toxicokinetics
1. Human Clinical Toxicity (Phase I Study): - In R/R AML patients treated with Iadademstat (ORY-1001) (20–600 mg/day), treatment-related adverse events (TRAEs) were mostly grade 1–2: - Common TRAEs (incidence >20%): nausea (42%), fatigue (38%), diarrhea (31%), vomiting (28%), and decreased appetite (22%). - Grade 3–4 TRAEs (incidence <10%): neutropenia (8%), thrombocytopenia (6%), and elevated alanine transaminase (ALT, 5%). - Dose-limiting toxicity (DLT): observed at 600 mg/day, consisting of grade 4 neutropenia (duration >7 days) in 2 out of 6 patients [1]
- Plasma protein binding: In human plasma, ORY-1001 showed high protein binding (>98%) as measured by equilibrium dialysis [1]
2. Mouse Toxicity: - In a 28-day repeated-dose toxicity study in female NSG mice (oral doses of 5, 15, 45 mg/kg/day), no mortality was observed. At 45 mg/kg/day, mild weight loss (<10%) and transient elevation of serum AST (1.5-fold above normal) were noted, with no histopathological changes in major organs (liver, kidney, bone marrow) [3]
References

[1]. First-in-Human Phase I Study of Iadademstat (ORY-1001): A First-in-Class Lysine-Specific Histone Demethylase 1A Inhibitor, in Relapsed or Refractory Acute Myeloid Leukemia. J Clin Oncol. 2020 Dec 20;38(36):4260-4273.

[2]. KDM1 histone lysine demethylases as targets for treatments of oncological and neurodegenerative disease. Epigenomics. 2015;7(4):609-26. doi: 10.2217/epi.15.9.

[3]. ORY-1001, a Potent and Selective Covalent KDM1A Inhibitor, for the Treatment of Acute Leukemia. Cancer Cell. 2018 Mar 12;33(3):495-511.e12.

[4]. J Clin Oncol. 2013, 31, suppl; abstr. e13543. http://meetinglibrary.asco.org/content/116240-132
Additional Infomation
1. Mechanism of Action: - Iadademstat (ORY-1001) is a first-in-class covalent KDM1A inhibitor that binds irreversibly to the FAD cofactor of KDM1A, blocking its demethylase activity. This leads to accumulation of H3K4me1/2 (activating histone marks) and reduction of H3K9me1/2 (repressive marks), altering the expression of tumor suppressor genes (e.g., p21) and oncogenes (e.g., MYC), thereby inhibiting AML cell proliferation and inducing apoptosis [3]
2. Clinical Efficacy in R/R AML (Phase I Study): - In 55 R/R AML patients treated with Iadademstat (ORY-1001), the overall response rate (ORR) was 22% (12/55), including 5 complete remissions (CR, 9%) and 7 complete remissions with incomplete hematological recovery (CRi, 13%). The median duration of response (DOR) was 5.8 months (range: 2.1–12.3 months) [1]
3. Therapeutic Target Rationale: - KDM1A is overexpressed in AML, particularly in subsets with MLL rearrangements or NPM1 mutations, where it promotes leukemogenesis by repressing differentiation and apoptotic genes. ORY-1001 targets this dependency, making it a promising agent for R/R AML [2][3]
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C15H22N2.2HCL
Molecular Weight
303.27
Exact Mass
302.131
Elemental Analysis
C, 59.41; H, 7.98; Cl, 23.38; N, 9.24
CAS #
1431326-61-2
Related CAS #
1431326-61-2 (2HCl) 1431303-72-8 (2HCl) 1431303-71-7 (xHCl) 1431304-21-0
PubChem CID
71664305
Appearance
Typically exists as solid at room temperature
Hydrogen Bond Donor Count
4
Hydrogen Bond Acceptor Count
2
Rotatable Bond Count
3
Heavy Atom Count
19
Complexity
239
Defined Atom Stereocenter Count
2
SMILES
N(C1CCC(CC1)N)[C@@H]1C[C@H]1C1C=CC=CC=1.Cl.Cl
InChi Key
UCINOBZMLCREGM-RNNUGBGQSA-N
InChi Code
InChI=1S/C15H22N2.2ClH/c16-12-6-8-13(9-7-12)17-15-10-14(15)11-4-2-1-3-5-11;;/h1-5,12-15,17H,6-10,16H2;2*1H/t12?,13?,14-,15+;;/m0../s1
Chemical Name
4-N-[(1R,2S)-2-phenylcyclopropyl]cyclohexane-1,4-diamine;dihydrochloride
Synonyms

ORY1001; RG 6016;ORY-1001; RG-6016;ORY1001; RG6016; ORY1001 dihydrochloride, ORY1001 HCl; ORY1001 2HCl salt.

HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 5 mg/mL (16.5 mM)
Water:61 mg/mL (201.1 mM)
Ethanol:4 mg/mL warmed (13.2 mM)
Solubility (In Vivo)

Chemical Name:(1r,4R)-N1-((1R,2S)-2-phenylcyclopropyl)cyclohexane-1,4-diamine dihydrochloride

InChi Key:UCINOBZMLCREGM-ISDLZHGDSA-N

InChi Code:InChI=1S/C15H22N2.2ClH/c16-12-6-8-13(9-7-12)17-15-10-14(15)11-4-2-1-3-5-11;;/h1-5,12-15,17H,6-10,16H2;2*1H/t12-,13-,14-,15+;;/m0../s1

SMILES Code:N[C@@H]1CC[C@@H](N[C@@H]2C[C@H]2C3=CC=CC=C3)CC1.[H]Cl.[H]Cl

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Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 3.2974 mL 16.4870 mL 32.9739 mL
5 mM 0.6595 mL 3.2974 mL 6.5948 mL
10 mM 0.3297 mL 1.6487 mL 3.2974 mL

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT05420636 Recruiting Drug: Iadademstat
Drug: Paclitaxel
Small-cell Lung Cancer
Neuroendocrine Carcinoma
Fox Chase Cancer Center December 21, 2022 Phase 2
NCT05546580 Recruiting Drug: Iadademstat
Drug: Gilteritinib Oral Tablet
Acute Myeloid Leukemia, in Relapse
Acute Myeloid Leukemia Refractory
Oryzon Genomics S.A. November 14, 2022 Phase 1
NCT06357182 Not yet recruiting NEW Drug: Azacitidine
Procedure: Biospecimen Collection
Acute Myeloid Leukemia
Myelodysplastic Syndrome/
Acute Myeloid Leukemia
OHSU Knight Cancer Institute May 8, 2024 Phase 1
NCT06287775 Not yet recruiting Biological: Atezolizumab
Procedure: Biopsy
Extensive Stage Lung Small Cell Carcinoma
Stage IV Lung Cancer AJCC v8
National Cancer Institute (NCI) May 24, 2024 Phase 1
Phase 2
Biological Data
  • Morphologic response to treatment with iadademstat. (A) Representative images of blood smears showing morphologic differentiation from patient 28 (top) at screening (left) and cycle 1(C1), day 21 (D21) (right) and patient 31 (bottom) at screening (left) and C1D14 (right; two images from the same slide and patient are shown, separated by a dotted line). Charts show results of morphologic analysis of (B) blood smears and (C) bone marrow smears from selected MLL-translocated patients in the extension cohort (EC). HB, hemoglobin; WCC, white cell count; PLT, platelets.
  • Molecular response to treatment with iadademstat. Relative gene expression levels in nucleated blood cells of a differentiation biomarker panel in the extension cohort (EC). Magenta values show gene upregulation and pink values show gene downregulation. The maximum response and its timing within the treatment period is shown. Data are expressed as −ΔΔCp, calculated relative to expression of the endogenous gene HPRT1 and to the predose sample. Information on the occurrence of blast cell differentiation in bone marrow (BM) or blood and the percentage variation is also shown. The final column shows blast percentage in peripheral blood at baseline. (a) In bone marrow and/or peripheral blood. (b) Grey background indicates chromosome alterations involving MLL; dark grey, MLL fusion. (c) Between D5 and D12 of treatment (patient 28) or between D15 and D29 of treatment (patient 32). (d) Differentiation syndrome diagnosed. Morph. differ., morphologic differentiation.
  • Hematologic and biomarker response in patient 16. (A) Absolute neutrophil count (ANC) and platelet dynamics after treatment (cycle 1) and during the washout period in patient 16 of cohort V. Time course of changes in expression of differentiation biomarkers analyzed by quantitative reverse transcriptase–polymerase chain reaction shows that iadademstat induced expression of (B) CD86, (C) VCAN, (D) S100A12, and (E) LY96 in blood cells of patient 16.
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