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Cilostazol (OPC-13013; OPC13013; OPC 13013)

Alias: OPC-13013;Cilostazol; Pletal; Cilostazolum; OPC 13013; OPC13013;Pletaal; Cilostazole;
Cat No.:V0791 Purity: ≥98%
Cilostazol(formerly OPC-13013; Pletal; Cilostazolum; Pletaal;OPC13013; OPC 13013),a potentvasodilator that acts by relaxing the muscles,is a selective cyclic nucleotide phosphodiesterase type 3 (PDE3) inhibitor with beneficial effects on learning impairment.
Cilostazol (OPC-13013; OPC13013; OPC 13013)
Cilostazol (OPC-13013; OPC13013; OPC 13013) Chemical Structure CAS No.: 73963-72-1
Product category: PDE
This product is for research use only, not for human use. We do not sell to patients.
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Other Forms of Cilostazol (OPC-13013; OPC13013; OPC 13013):

  • Cilostazol-d11 (cilostazol d11)
  • Cilostazol-d4
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Cilostazol (formerly OPC-13013; Pletal; Cilostazolum; Pletaal; OPC13013; OPC 13013), a potent vasodilator that acts by relaxing the muscles, is a selective cyclic nucleotide phosphodiesterase type 3 (PDE3) inhibitor with beneficial effects on learning impairment. It inhibits PDE3 with an IC50 of 0.2 μM and inhibitor of adenosine uptake.

Biological Activity I Assay Protocols (From Reference)
Targets
PDE 3A (IC50 = 0.2 μM)
ln Vitro
Cilostazol is a strong inhibitor of platelet aggregation brought on by different agonists and specifically inhibits cGMP-inhibited phosphodiesterase (PDE 3) [2]. With an IC50 of 15 μM for stress-induced human platelet aggregation and 12.5 μM for ADP-induced platelet aggregation, clostazol inhibits both types of human platelet aggregation in a dose-dependent manner [2]. Cilostazol inhibits HSC activation directly and effectively, but not Kupffer cell activation [3].
ln Vivo
In vivo liver fibrosis caused by CCl4 is lessened by clostazol (clinical dosage; oral administration for 2 weeks); this effect may be attributed to direct inhibition of HSC activation [3]. Intraperitoneal injection of cilostazol (10 mg/kg given over 7 days) reduces neurological deficits, brain atrophy, and infarct size. It also prevents astrocyte proliferation and glial scarring during ischemia. After 7 and 28 days, angiogenesis in the ischemic border zone accelerates [4].
Enzyme Assay
Cilostazol is a selective and potent inhibitor of phosphodiesterase (PDE) 3A (IC50: 0.2 µm), the cardiovascular subtype of PDE 3. At therapeutic plasma levels of about 3–5 µm, the compound does not affect other PDEs; however, the local tissue levels of the compound might be higher than the free concentration in plasma because of the lipophilicity of the drug. Importantly, there is no relevant effect by cilostazol on PDE 1, 2 and 4 at comparable concentrations, and only a minor effect on PDE 5 (IC50: 5–8 µm). PDE 3 increases the breakdown of cAMP. Since both platelets and vascular smooth muscle cells contain PDE 3A, this mechanism appears to explain the inhibition of platelet function as well as the vasodilatory effects [1].
More recently, another pharmacological property of cilostazol has been detected: inhibition of adenosine uptake. This leads to enhanced adenosine actions via A1 and A2-receptors. In platelets and vascular cells, A2-mediated increases in cAMP enhance the consequences of PDE-inhibition, i.e. result in additional increases in cAMP. In cardiocytes, carrying the A1-receptor subtype, there will be a Gi-mediated inhibition of adenylate cyclase with subsequent reduction in cAMP (Fig. 2). Whether this concept works in vivo, is currently unknown. According to current knowledge, the actions of cilostazol that are most important for its clinical efficacy involve effects on platelets and vascular cells[1].
Cell Assay
To investigate the effects of cilostazol on hepatic cells, in vitro studies were conducted using primary hepatic stellate cells (HSC), Kupffer cells and hepatocytes with cilostazol supplementation.[3]
Cilostazol relaxes vascular smooth muscle and causes vasodilatation. Both, PDE-inhibition and possibly inhibition of adenosine uptake, may act in concert. Interestingly, cilostazol also inhibits the cytokine-induced expression of monocyte chemoattractant protein-1 (MCP-1). MCP-1 plays a significant role in mediating monocyte recruitment in atherosclerotic lesions. This effect is also probably due to cAMP elevation and might contribute to an anti-inflammatory action of the compound. A recent study in patients with noninsulin-dependent diabetes mellitus has shown that oral treatment with cilostazol for 4 weeks significantly reduced the concentration of soluble adhesion molecules in the blood, probably indicating a vasoprotective action. In addition, there was a reduction in serum-triglyceride levels by cilostazol in patients with intermittent claudication together with an increase in treadmill walking time. All these data suggest an improved clinical situation for patients after treatment with cilostazol[1].
Animal Protocol
Animal/Disease Models: Male C57BL/6J mice[3]
Doses: 0.1% w/w, 0.3% w/w
Route of Administration: Oral administration; fed a normal diet for 2 weeks
Experimental Results: demonstrated a lesser fibrotic area than control groups.

Animal/Disease Models: Male ICR mice[4]
Doses: 10 mg/kg
Route of Administration: intraperitoneal (ip)injection; 7 days after ischemia
Experimental Results: Had an effectve effects for the late injury.
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Cilostazol is absorbed after oral administration. A high fat meal increases absorption, with an approximately 90% increase in Cmax and a 25% increase in AUC. Absolute bioavailability is not known.
Cilostazol is extensively metabolized by hepatic cytochrome P-450 enzymes, mainly 3A4, and, to a lesser extent, 2C19, with metabolites largely excreted in urine. Cilostazol is eliminated predominately by metabolism and subsequent urinary excretion of metabolites. The primary route of elimination was via the urine (74%), with the remainder excreted in feces (20%). No measurable amount of unchanged cilostazol was excreted in the urine, and less than 2% of the dose was excreted as 3,4-dehydro-cilostazol. About 30% of the dose was excreted in urine as 4'-trans-hydroxy-cilostazol.
/MILK/ Transfer of cilostazol into milk has been reported in rats.
Following oral administration of a single 100-mg dose of cilostazol with a high-fat meal, peak plasma cilostazol concentrations and area under the plasma concentration-time curve (AUC) increased by approximately 90 and 25%, respectively.
Pletal is absorbed after oral administration. A high fat meal increases absorption, with an approximately 90% increase in Cmax and a 25% increase in AUC. Absolute bioavailability is not known.
The primary route of elimination was via the urine (74%), with the remainder excreted in feces (20%). No measurable amount of unchanged cilostazol was excreted in the urine, and less than 2% of the dose was excreted as 3,4-dehydro-cilostazol. About 30% of the dose was excreted in urine as 4'-trans-hydroxy-cilostazol. The remainder was excreted as other metabolites, none of which exceeded 5%. There was no evidence of induction of /microsomal enzymes/.
For more Absorption, Distribution and Excretion (Complete) data for Cilostazol (7 total), please visit the HSDB record page.
Metabolism / Metabolites
Hepatic. Cilostazol is extensively metabolized by hepatic cytochrome P-450 enzymes, mainly 3A4, and, to a lesser extent, 2C19, with metabolites largely excreted in urine. Two metabolites are active, with one metabolite appearing to account for at least 50% of the pharmacologic (PDE III inhibition) activity after administration of cilostazol.
Following oral administration of 100 mg radiolabeled cilostazol, 56% of the total analytes in plasma was cilostazol, 15% was 3,4-dehydro-cilostazol (4-7 times as active as cilostazol), and 4% was 4'-trans-hydroxy-cilostazol (20% as active as cilostazol).
Cilostazol is eliminated predominantly by metabolism and subsequent urinary excretion of metabolites. Based on in vitro studies, the primary isoenzymes involved in cilostazol's metabolism are CYP3A4 and, to a lesser extent, CYP2C19. The enzyme responsible for metabolism of 3,4-dehydro-cilostazol, the most active of the metabolites, is unknown.
Cilostazol is extensively metabolized by hepatic cytochrome P-450 enzymes, mainly 3A4, and, to a lesser extent, 2C19, with metabolites largely excreted in urine. Two metabolites are active, with one metabolite appearing to account for at least 50% of the pharmacologic (PDE III inhibition) activity after administration of Pletal.
The pharmacokinetics of cilostazol was investigated after oral and intravenous administration in both male and female rats. After oral administration, area under serum concentration-time curve (AUC) was about 35-fold higher in female rats than in male rats, and absolute bioavailability was about 5.8-fold higher in female rats than in male rats. Total body clearance (CL(total)) for female rats was around one-sixth of that for male rats. In vivo hepatic clearance (CL(h)) calculated based on isolated liver perfusion studies was even higher than or around 90% of the in vivo CL(total) of cilostazol for female and male rats, respectively, indicating that cilostazol is mainly eliminated by the liver in both male and female rats. In vitro metabolism studies utilizing hepatic microsomes and recombinant cytochrome (CYP) isoforms clearly indicated that major metabolites of cilostazol were generated extensively with hepatic microsomes of male rats and that male-predominant CYP3A2 and male-specific CYP2C11 were mainly responsible for the hepatic metabolism of cilostazol. Therefore, the great sex differences in the pharmacokinetics of cilostazol were mainly attributed to the large difference in hepatic metabolism. Our experimental results also suggested that the substantial metabolism of cilostazol in the small intestine and its possible saturation would be responsible for dose-dependent bioavailability in both male and female rats.
The primary route of elimination was via the urine (74%), with the remainder excreted in feces (20%). No measurable amount of unchanged cilostazol was excreted in the urine, and less than 2% of the dose was excreted as 3,4-dehydro-cilostazol. About 30% of the dose was excreted in urine as 4'-trans-hydroxy-cilostazol. The remainder was excreted as other metabolites, none of which exceeded 5%. There was no evidence of induction of /microsomal enzymes/.
Cilostazol has known human metabolites that include OPC-13217 and OPC-13326.
Biological Half-Life
11-13 hours.
Cilostazol and its active metabolites have apparent elimination half-lives of about 11-13 hours.
Toxicity/Toxicokinetics
Toxicity Summary
IDENTIFICATION AND USE: Cilostazol forms colorless, needle-like crystals. As the oral drug Pletal, it is indicated for the reduction of symptoms of intermittent claudication. HUMAN EXPOSURE AND TOXICITY: The signs and symptoms of an acute overdose may include severe headache, diarrhea, hypotension, tachycardia, and possibly cardiac arrhythmias. ANIMAL STUDIES: No cardiovascular lesions were seen in rats following 5 or 13 weeks of administration of cilostazol at doses up to 1500 mg/kg/day. At this dose, systemic exposures (AUCs) to unbound cilostazol were only about 1.5 and 5 times (male and female rats, respectively) the exposure seen in humans at the maximum recommended human dose (MRHD). Repeated oral administration of cilostazol to dogs produced cardiovascular lesions that included endocardial hemorrhage, hemosiderin deposition and fibrosis in the left ventricle, hemorrhage in the right atrial wall, hemorrhage and necrosis of the smooth muscle in the wall of the coronary artery, intimal thickening of the coronary artery, and coronary arteritis and periarteritis. At the lowest dose associated with cardiovascular lesions in the 52-week study, AUC to unbound cilostazol was less than that seen in humans at the MRHD of 100 mg twice daily. In a rat developmental toxicity study, oral administration of 1000 mg cilostazol/kg/day was associated with decreased fetal weights, and increased incidences of cardiovascular, renal, and skeletal anomalies (ventricular septal, aortic arch and subclavian artery abnormalities, renal pelvic dilation, 14th rib, and retarded ossification). Cilostazol tested negative in bacterial gene mutation, bacterial DNA repair, mammalian cell gene mutation, and mouse in vivo bone marrow chromosomal aberration assays. It was, however, associated with a significant increase in chromosomal aberrations in the in vitro Chinese Hamster Ovary Cell assay. Dietary administration of cilostazol to rats and mice for up to 104 weeks revealed no evidence of carcinogenic potential. The maximum doses administered in both rat and mouse studies were, on a systemic exposure basis, less than the human exposure at the MRHD of the drug.
Hepatotoxicity
In publications of the multiple, large prospective trials of cilostazol therapy, rates of serum ALT elevations during therapy were not provided. Furthermore, there were no reported instances of clinically apparent acute liver injury. Since its approval and wide scale use, there have been no published reports of hepatotoxicity attributed to cilostazol. Nevertheless, the current product label mentions that instances of serum enzyme elevations and hepatitis have been reported to the sponsor. The time of onset, clinical pattern and course of liver test abnormalities during cilostazol therapy have not been reported.
Likelihood score: E (unlikely cause of clinically apparent liver injury).
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because no information is available on the use of cilostazol during breastfeeding, an alternate drug may be preferred, especially while nursing a newborn or preterm infant. If it is used by a nursing mother, monitor the infant for bruising and bleeding.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
95-98%
Interactions
Pharmacokinetic interaction (increased plasma concentrations of active metabolite 3,4-dehydro-cilostazol) with CYP2C19 inhibitors, including omeprazole; use with caution and consider reduced dosage.
Potential pharmacokinetic interaction (increased plasma lovastatin concentrations and decreased plasma cilostazol concentration) with lovastatin, a substrate for CYP3A4, although unlikely to be clinically important.
Pharmacokinetic interaction (increased plasma cilostazol concentrations); use with caution and consider reduced dosage. Potential pharmacokinetic interaction (increased plasma cilostazol concentrations, decreased clearance) with other inhibitors of CYP3A4 isoenzyme, including, but not limited to, certain azole antifungals (e.g., fluconazole, itraconazole, ketoconazole, miconazole), certain macrolide antibiotics (e.g., erythromycin or clarithromycin but not azithromycin), certain selective serotonin-reuptake inhibitors (e.g., fluoxetine, fluvoxamine, nefazodone, sertraline), certain antiretroviral agents (e.g., indinavir), metronidazole, diltiazem, and danazol.
Potentially additive antiplatelet effects with clopidogrel and cilostazol. Caution is advised and bleeding times should be monitored during such concomitant therapy. Pharmacokinetic interaction unlikely.
For more Interactions (Complete) data for Cilostazol (10 total), please visit the HSDB record page.
Non-Human Toxicity Values
LD50 Dog oral > 2 g/kg
LD50 Rat oral > 5 g/kg
LD50 Mouse oral > 5 g/kg
References

[1]. Schr?r K. The pharmacology of cilostazol. Diabetes Obes Metab. 2002 Mar;4 Suppl 2:S14-9.

[2]. Inhibition of shear stress-induced platelet aggregation by cilostazol, a specific inhibitor of cGMP-inhibited phosphodiesterase, in vitro and ex vivo. Life Sci. 1997;61(25):PL 383-9.

[3]. Cilostazol attenuates hepatic stellate cell activation and protects mice against carbon tetrachloride-induced liver fibrosis. Hepatol Res. 2013 Apr 19.

[4]. Cilostazol, a phosphodiesterase 3 inhibitor, protects mice against acute and late ischemic brain injuries.Eur J Pharmacol. 2007 Feb 14;557(1):23-31. Epub 2006 Nov 10.

Additional Infomation
Therapeutic Uses
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Cilostazol is included in the database.
Pletal is indicated for the reduction of symptoms of intermittent claudication, as demonstrated by an increased walking distance. /Included in US product label/
Because of its antiplatelet activity, cilostazol has been used alone or in combination with other antiplatelet agents (e.g., aspirin, clopidogrel) to prevent thrombosis and restenosis following coronary angioplasty/stent implantation. /NOT included in US product label/
Cilostazol has been used for the secondary prevention of stroke in patients with a history of noncardioembolic stroke or transient ischemic attacks (TIAs). /NOT included in US product label/
/EXPL THER/ We conducted a randomized, double blind, placebo controlled trial to assess the efficacy and safety of cilostazol, a selective inhibitor of phosphodiesterase 3, in patients with vasospastic angina (VSA). Cilostazol has been shown to induce vascular dilatation, but its efficacy in patients with VSA is unknown. Between October 2011 and July 2012, 50 patients with confirmed VSA who had >/= 1 angina episodes/week despite amlodipine therapy (5 mg/day) were randomly assigned to receive either cilostazol (up to 200 mg/day) or placebo for 4 weeks. All patients were given diaries to record the frequency and severity of chest pain (0-10 grading). The primary endpoint was the relative reduction of the weekly incidence of chest pain. Baseline characteristics were similar between the two groups. Among 49 evaluable patients (25 in the cilostazol group, 24 in the placebo group), the primary endpoint was significantly greater in the cilostazol group compared with the placebo group (-66.5 +/- 88.6% vs -17.6 +/- 140.1%, respectively, p=0.009). The secondary endpoints, including a change in the frequency of chest pain (-3.7 +/- 0.5 vs -1.9 +/- 0.6, respectively, p=0.029), a change in the chest pain severity scale (-2.8 +/- 0.4 vs -1.1 +/- 0.4, respectively, p=0.003), and the proportion of chest pain-free patients (76.0% vs 33.3%, respectively, p=0.003) also significantly favoured cilostazol. Headache was the most common adverse event in both groups (40.0% vs 20.8%, respectively, p=0.217). Cilostazol is an effective therapy for patients with VSA uncontrolled by conventional amlodipine therapy, and has no serious side effects.
Drug Warnings
/BOXED WARNING/ WARNING: CONTRAINDICATED IN HEART FAILURE PATIENTS. Pletal is contraindicated in patients with heart failure of any severity. Cilostazol and several of its metabolites are inhibitors of phosphodiesterase III. Several drugs with this pharmacologic effect have caused decreased survival compared to placebo in patients with class III-IV heart failure.
Rare cases of thrombocytopenia or leukopenia progressing to agranulocytosis have been reported when cilostazol was not immediately discontinued; agranulocytosis was reversible with discontinuance of cilostazol.
Information is limited regarding the safety and efficacy of concurrent use of cilostazol and clopidogrel. Currently it is unknown whether concurrent therapy with cilostazol and clopidogrel has additive effects on bleeding time. Caution should be used and bleeding times monitored during such concurrent therapy.
Cilostazol may induce tachycardia, palpitation, tachyarrhythmia or hypotension. The increase in heart rate associated with cilostazol is approximately 5 to 7 bpm. Patients with a history of ischemic heart disease may be at risk for exacerbations of angina pectoris or myocardial infarction.
For more Drug Warnings (Complete) data for Cilostazol (10 total), please visit the HSDB record page.
Pharmacodynamics
Cilostazol reduces the symptoms of intermittent claudication, as indicated by an increased walking distance. Intermittent claudication is pain in the legs that occurs with walking and disappears with rest. The pain occurs due to reduced blood flow to the legs.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C20H27N5O2
Molecular Weight
369.46
Exact Mass
369.216
Elemental Analysis
C, 57.08; H, 6.46; Cl, 7.33; F, 3.93; N, 8.68; O, 16.53
CAS #
73963-72-1
Related CAS #
Cilostazol-d11;1073608-02-2;Cilostazol-d4;1215541-47-1
PubChem CID
2754
Appearance
White to off-white solid powder
Density
1.3±0.1 g/cm3
Boiling Point
664.7±55.0 °C at 760 mmHg
Melting Point
159-160ºC
Flash Point
355.8±31.5 °C
Vapour Pressure
0.0±2.0 mmHg at 25°C
Index of Refraction
1.676
LogP
3.05
Hydrogen Bond Donor Count
1
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
7
Heavy Atom Count
27
Complexity
485
Defined Atom Stereocenter Count
0
SMILES
O=C1NC2=C(C=C(OCCCCC3=NN=NN3C4CCCCC4)C=C2)CC1
InChi Key
RRGUKTPIGVIEKM-UHFFFAOYSA-N
InChi Code
InChI=1S/C20H27N5O2/c26-20-12-9-15-14-17(10-11-18(15)21-20)27-13-5-4-8-19-22-23-24-25(19)16-6-2-1-3-7-16/h10-11,14,16H,1-9,12-13H2,(H,21,26)
Chemical Name
6-[4-(1-cyclohexyltetrazol-5-yl)butoxy]-3,4-dihydro-1H-quinolin-2-one
Synonyms
OPC-13013;Cilostazol; Pletal; Cilostazolum; OPC 13013; OPC13013;Pletaal; Cilostazole;
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: 74 mg/mL (200.3 mM)
Water:<1 mg/mL
Ethanol: 6 mg/mL warmed (16.2 mM)
Solubility (In Vivo)
Solubility in Formulation 1: 2 mg/mL (5.41 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

Solubility in Formulation 2: ≥ 2 mg/mL (5.41 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.7067 mL 13.5333 mL 27.0665 mL
5 mM 0.5413 mL 2.7067 mL 5.4133 mL
10 mM 0.2707 mL 1.3533 mL 2.7067 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT01915069 Completed Drug: Cilostazol Contraception University of Southern California July 2013 Phase 2
NCT05671497 Recruiting Drug: Cilostazol 100 MG Rheumatoid Arthritis Ain Shams University November 1, 2022 Phase 2
Phase 3
NCT02374957 Terminated Has Results Drug: Cilostazol Peripheral Arterial Disease
Claudication (Finding)
Wake Forest University Health Sciences February 2015 Phase 4
NCT05126836 Completed Has Results Drug: Cilostazol 100Mg Tab
Drug: Placebo
Heart Failure With Preserved
Ejection Fraction
University of Minnesota September 1, 2021 Phase 2
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