zipsor
Zipsor (Diclofenac Potassium) is a nonsteroidal anti-inflammatory drug used to treat Juvenile Arthritis, Rheumatoid Arthritis, Dysmenorrhea, Inflammation.
Diclofenac Potassium · by Assertio Speclty
Available as a generic: Diclofenac Potassium
Key facts
- Active ingredient
- Diclofenac Potassium
- Drug class
- Nonsteroidal Anti-Inflammatory Drug
- Form
- Capsule
- Strength
- Diclofenac Potassium 25MG
- Type
- Prescription (Rx)
- Brand or generic
- Brand-name
- May treat
- juvenile arthritis, rheumatoid arthritis, dysmenorrhea
- Manufacturer
- Assertio Speclty
- Half-life
- about 2 hours (terminal/elimination half-life; the label's table gives a mean of 2.3 hours in healthy adults, with wide variation between people — 48% coefficient of variation) (how long it stays in your system)
- What the pharmacy pays
- ~$0.36 per ml — not your price
- FDA application
- NDA022202
- FDA boxed warning
- Yes — see the boxed warning
What is Zipsor?
From the FDA label:Diclofenac Potassium Capsule is a nonsteroidal anti-inflammatory drug, available as liquid-filled capsules of 25 mg for oral administration. Diclofenac potassium is a white to slight yellowish crystalline powder. It is sparingly soluble in water at 25ºC. The chemical name is benzeneacetic acid, 2-[(2,6-dichlorophenyl) amino]-, monopotassium salt. The molecular weight is 334.24. Its molecular formula is C 14 H 10 Cl 2 NKO 2 , and it has the following chemical structure. The inactive ingredients in Diclofenac Potassiuminclude: ProSorb ® (a proprietary combination of polyethylene glycol 400, glycerin, sorbitol, povidone, polysorbate 80, and hydrochloric acid), isopropyl alcohol, and mineral oil. The capsule shells contain gelatin, sorbitol, isopropyl alcohol, glycerin, and mineral oil. chemstructure
How to use
Use the lowest effective dosage for shortest duration consistent with individual patient treatment goals ( 2.1) The dosage is 25 mg four times a day 2.1 General Dosing Instructions Carefully consider the potential benefits and risks of Diclofenac Potassium and other treatment options before deciding to use Diclofenac Potassium. Use the lowest effective dosage for the shortest duration consistent with individual patient treatment goals [see Warnings and Precautions (5) ]. For treatment of mild to moderate acute pain in adult and pediatric patients 12 years of age and older, the dosage is 25 mg four times a day. 2.2 Dosage Adjustments in Patients with Hepatic Impairment Patients with hepatic disease may require reduced doses of Diclofenac Potassium compared to patients with normal hepatic function [see Clinical Pharmacology (12) ]. As with other diclofenac products, start treatment at the lowest dose. If efficacy is not achieved with the lowest dose, discontinue use. 2.3 Non-Interchangeability with Other Formulations of Diclofenac Different dose strengths and formulations of oral diclofenac are not interchangeable. This difference should be taken into consideration when changing strengths or formulations. The only approved dosing regimen for Diclofenac Potassium is 25 mg four times a day. 2.1 General Dosing Instructions Carefully consider the potential benefits and risks of…
Side effects
The following adverse reactions are discussed in greater detail in other sections of the labeling: Cardiovascular Thrombotic Events [see Warnings and Precautions (5.1) ] GI Bleeding, Ulceration and Perforation [see Warnings and Precautions (5.2) ] Hepatotoxicity [see Warnings and Precautions (5.3) ] Hypertension [see Warnings and Precautions (5.4 )] Heart Failure and Edema [see Warnings and Precautions (5.5) ] Renal Toxicity and Hyperkalemia [see Warnings and Precautions (5.6) ] Anaphylactic Reactions [see Warnings and Precautions (5.7) ] Serious Skin Reactions [see Warnings and Precautions (5.9) ] Hematologic Toxicity [see Warnings and Precautions (5.11) ] Most common adverse reactions (incidence ≥ 1%) are gastrointestinal experiences including abdominal pain, constipation, diarrhea, dyspepsia, nausea, vomiting, dizziness, headache, somnolence, pruritus, and increased sweating (6.1) To report SUSPECTED ADVERSE REACTIONS, contact Leading Pharma, LLC at 1-844-740-7500 or FDA at 1-800-FDA-1088 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch. 6.1 Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in clinical trials of a drug cannot be directly compared with the rates in clinical trials of another drug and may not reflect the rates observed in practice. The safety of Diclofenac Potassiumwas evaluated…
FDA Boxed Warning (the FDA’s most serious warning)
Boxed (black-box) warning — from the FDA label
Cardiovascular Thrombotic Events Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use [see Warnings and Precautions (5.1) ] . Diclofenac Potassium is contraindicated in the setting of coronary artery bypass graft (CABG) surgery [see Contraindications (4) and Warnings and Precautions (5.1) ]. Gastrointestinal Bleeding, Ulceration, and Perforation NSAIDs cause an increased risk of serious gastrointestinal (GI) adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients and patients with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events [see Warnings and Precautions (5.2) ] . WARNING: RISK OF SERIOUS CARDIOVASCULAR AND GASTROINTESTINAL EVENTS See full prescribing information for complete boxed warning. Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. This risk may occur early in treatment and may increase with duration of use (5.1) Diclofenac potassium is contraindicated in the setting of coronary artery bypass graft (CABG) surgery (4 , 5.1 ) NSAIDs cause an increased risk of serious gastrointestinal (GI) adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients and patients with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events (5.2)
Warnings
Important safety information
Hepatotoxicity : Inform patients of warning signs and symptoms of hepatotoxicity. Discontinue if abnormal liver tests persist or worsen or if clinical signs and symptoms of liver disease develop (5.3 ) Hypertension : Patients taking some antihypertensive medications may have impaired response to these therapies when taking NSAIDs. Monitor blood pressure ( 5.4 , 7 ) Heart Failure and Edema: Avoid use of Diclofenac Potassium in patients with severe heart failure unless benefits are expected to outweigh risk of worsening heart failure (5.5) Renal Toxicity: Monitor renal function in patients with renal or hepatic impairment, heart failure, dehydration, or hypovolemia. Avoid use of Diclofenac Potassium in patients with advanced renal disease unless benefits are expected to outweigh risk of worsening renal function (5.6) Anaphylactic Reactions: Seek emergency help if an anaphylactic reaction occurs (5.7) Exacerbation of Asthma Related to Aspirin Sensitivity: Diclofenac Potassium is contraindicated in patients with aspirin-sensitive asthma. Monitor patients with preexisting asthma (without aspirin sensitivity) (5.8) Serious Skin Reactions: Discontinue Diclofenac Potassium at first appearance of skin rash or other signs of hypersensitivity ( 5.9) Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): Discontinue and evaluate clinically ( 5.10 ). Fetal Toxicity: Limit use of NSAIDs, including Diclofenac Potassium, between about 20 to 30 weeks in pregnancy due to the risk of oligohydramnios/fetal renal dysfunction. Avoid use of NSAIDs in women at about 30 weeks gestation and later in pregnancy due to the risks of oligohydramnios/fetal renal dysfunction and premature closure of the fetal ductus arteriosus ( 5.11 , 8.1 ). Hematologic Toxicity : Monitor hemoglobin or hematocrit in patients with any signs or symptoms of anemia ( 5.12 , 7 ) 5.1 Cardiovascular Thrombotic Events Clinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increased risk of serious cardiovascular (CV) thrombotic events, including myocardial infarction (MI) and stroke, which can be fatal. Based on available data, it is unclear that the risk for CV thrombotic events is similar for all NSAIDs. The relative increase in serious CV thrombotic events over baseline conferred by NSAID use appears to be similar in those with and without known CV disease or risk factors for CV disease. However, patients with known CV disease or risk factors had a higher absolute incidence of excess serious CV thrombotic events, due to their increased baseline rate. Some observational studies found that this increased risk of serious CV thrombotic events began as early as the first weeks of treatment. The increase in CV thrombotic risk has been observed most consistently at higher doses. To minimize the potential risk for an adverse CV event in NSAID-treated patients, use the lowest effective dose for the shortest duration possible. Physicians and patients should remain alert for the development of such events, throughout the entire treatment course, even in the absence of previous CV symptoms. Patients should be informed about the symptoms of serious CV events and the steps to take if they occur. There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. The concurrent use of aspirin and an NSAID, such as diclofenac, increases the risk of serious gastrointestinal (GI) events [see Warnings and Precautions (5.2) ]. Status Post Coronary Artery Bypass Graft (CABG) Surgery Two large, controlled clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10-14 days following CABG surgery found an increased incidence of myocardial infarction and stroke. NSAIDs are contraindicated in the setting of CABG [see Contraindications (4) ]. Post-MI Patients Observational studies conducted in the Danish National Registry have demonstrated that patients treated with NSAIDs in the post-MI period were at increased risk of reinfarction, CV-related death, and all-cause mortality beginning in the first week of treatment. In this same cohort, the incidence of death in the first year post-MI was 20 per 100 person years in NSAID-treated patients compared to 12 per 100 person years in non-NSAID exposed patients. Although the absolute rate of death declined somewhat after the first year post-MI, the increased relative risk of death in NSAID users persisted over at least the next four years of follow-up. Avoid the use of Diclofenac Potassium in patients with a recent MI unless the benefits are expected to outweigh the risk of recurrent CV thrombotic events. If Diclofenac Potassium is used in patients with a recent MI, monitor patients for signs of cardiac ischemia. 5.2 Gastrointestinal Bleeding, Ulceration, and Perforation NSAIDs, including diclofenac, cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients who develop a serious upper GI adverse event on NSAID therapy is symptomatic. Upper GI ulcers, gross bleeding, or perforation caused by NSAIDs occurred in approximately 1% of patients treated for 3-6 months, and in about 2%-4% of patients treated for one year. However, even short-term NSAID therapy is not without risk. Risk Factors for GI Bleeding, Ulceration, and Perforation Patients with a prior history of peptic ulcer disease and/or GI bleeding who used NSAIDs had a greater than 10-fold increased risk for developing a GI bleed compared to patients without these risk factors. Other factors that increase the risk of GI bleeding in patients treated with NSAIDs include longer duration of NSAID therapy; concomitant use of oral corticosteroids, aspirin, anticoagulants, or selective serotonin reuptake inhibitors (SSRIs); smoking; use of alcohol; older age; and poor general health status. Most postmarketing reports of fatal GI events occurred in elderly or debilitated patients. Additionally, patients with advanced liver disease and/or coagulopathy are at increased risk for GI bleeding. Strategies to Minimize the GI Risks in NSAID-treated patients: Use the lowest effective dosage for the shortest possible duration. Avoid administration of more than one NSAID at a time. Avoid use in patients at higher risk unless benefits are expected to outweigh the increased risk of bleeding. For such patients, as well as those with active GI bleeding, consider alternate therapies other than NSAIDs. Remain alert for signs and symptoms of GI ulceration and bleeding during NSAID therapy. If a serious GI adverse event is suspected, promptly initiate evaluation and treatment, and discontinue Diclofenac Potassium until a serious GI adverse event is ruled out. In the setting of concomitant use of low-dose aspirin for cardiac prophylaxis, monitor patients more closely for evidence of GI bleeding [see Drug Interactions (7 )]. 5.2 Gastrointestinal Bleeding, Ulceration, and Perforation NSAIDs, including diclofenac, cause serious gastrointestinal (GI) adverse events including inflammation, bleeding, ulceration, and perforation of the esophagus, stomach, small intestine, or large intestine, which can be fatal. These serious adverse events can occur at any time, with or without warning symptoms, in patients treated with NSAIDs. Only one in five patients who develop a serious upper GI adverse event on NSAID therapy is symptomatic. Upper GI ulcers, gross bleeding, or perforation caused by NSAIDs occurred in approximately 1% of patients treated for 3-6 months, and in about 2%-4% of patients treated for one year. However, even short-term NSAID therapy is not without risk. Risk Factors for GI Bleeding, Ulceration, and…
Who should not take Zipsor
Diclofenac Potassium is contraindicated in the following patients: Known hypersensitivity (e.g., anaphylactic reactions and serious skin reactions) to diclofenac or any components of the drug product [see Warnings and Precautions (5.7 , 5.9 )] History of asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs. Severe, sometimes fatal, anaphylactic reactions to NSAIDs have been reported in such patients [see Warnings and Precautions (5.7 , 5.8 )] In the setting of coronary artery bypass graft (CABG) surgery [see Warnings and Precautions (5.1) ] Diclofenac Potassium contains gelatin and is contraindicated in patients with known hypersensitivity to bovine protein. Known hypersensitivity to diclofenac or any components of the drug product (4) History of asthma, urticaria, or other allergic-type reactions after taking aspirin or other NSAIDs (4) In the setting of CABG surgery (4) Diclofenac Potassium contains gelatin and should not be given to patients with known hypersensitivity to bovine protein. (4)
Overdose — what happens if you take too much
Symptoms following acute NSAID overdosages have been typically limited to lethargy, drowsiness, nausea, vomiting, and epigastric pain, which have been generally reversible with supportive care. Gastrointestinal bleeding has occurred. Hypertension, acute renal failure, respiratory depression, and coma have occurred, but were rare [see Warnings and Precautions (5.1 , 5.2 , 5.4 , 5.6 )]. Manage patients with symptomatic and supportive care following an NSAID overdosage. There are no specific antidotes. Consider emesis and/or activated charcoal (60 to 100 grams in adults, 1 to 2 grams per kg of body weight in pediatric patients) and/or osmotic cathartic in symptomatic patients seen within four hours of ingestion or in patients with a large overdosage (5 to 10 times the recommended dosage). Forced diuresis, alkalinization of urine, hemodialysis, or hemoperfusion may not be useful due to high protein binding. For additional information about overdosage treatment contact a poison control center (1-800- 222-1222).
U.S. Poison Control: call or text 1-800-222-1222 (free, 24/7). In an emergency call 911. From the FDA label; not medical advice.
Interactions
See Table 2 for clinically significant drug interactions with diclofenac. Table 2: Clinically Significant Drug Interactions with diclofenac Drugs That Interfere with Hemostasis Clinical Impact: Diclofenac and anticoagulants such as warfarin have a synergistic effect on bleeding. The concomitant use of diclofenac and anticoagulants have an increased risk of serious bleeding compared to the use of either drug alone. Serotonin release by platelets plays an important role in hemostasis. Case-control and cohort epidemiological studies showed that concomitant use of drugs that interfere with serotonin reuptake and an NSAID may potentiate the risk of bleeding more than an NSAID alone. Intervention: Monitor patients with concomitant use of Diclofenac Potassium with anticoagulants (e.g., warfarin), antiplatelet agents (e.g., aspirin), selective serotonin reuptake inhibitors (SSRIs), and serotonin norepinephrine reuptake inhibitors (SNRIs) for signs of bleeding [see Warnings and Precautions (5.11) ] . Aspirin Clinical Impact: Controlled clinical studies showed that the concomitant use of NSAIDs and analgesic doses of aspirin does not produce any greater therapeutic effect than the use of NSAIDs alone. In a clinical study, the concomitant use of an NSAID and aspirin was associated with a significantly increased incidence of GI adverse reactions as compared to use of the NSAID alone [see Warnings and Precautions (5.2) ] . Intervention: Concomitant use of Diclofenac Potassium and analgesic doses of aspirin is not generally recommended because of the increased risk of bleeding [see Warnings and Precautions (5.11) ] . Diclofenac Potassium is not a substitute for low dose aspirin for cardiovascular protection. ACE Inhibitors, Angiotensin Receptor Blockers, and Beta-Blockers Clinical Impact: NSAIDs may diminish the antihypertensive effect of angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), or beta-blockers (including propranolol). In patients who are elderly, volume-depleted (including those on diuretic therapy), or have renal impairment, co-administration of an NSAID with ACE inhibitors or ARBs may result in deterioration of renal function, including possible acute renal failure. These effects are usually reversible. Intervention: During concomitant use of Diclofenac Potassium and ACE-inhibitors, ARBs, or beta-blockers, monitor blood pressure to ensure that the desired blood pressure is obtained. During concomitant use of Diclofenac Potassium and ACE-inhibitors or ARBs in patients who are elderly, volume-depleted, or have impaired renal function, monitor for signs of worsening renal function [see Warnings and Precautions (5.6) ] . When these drugs are administered concomitantly, patients should be adequately hydrated. Assess renal function at the beginning of the concomitant treatment and periodically thereafter. Diuretics Clinical Impact: Clinical studies, as well as post-marketing observations, showed that NSAIDs reduced the natriuretic effect of loop diuretics (e.g., furosemide) and thiazide diuretics in some patients. This effect has been attributed to the NSAID inhibition of renal prostaglandin synthesis. Intervention: During concomitant use of Diclofenac Potassium with diuretics, observe patients for signs of worsening renal function, in addition to assuring diuretic efficacy including antihypertensive effects [see Warnings and Precautions (5.6) ] . Digoxin Clinical Impact: The concomitant use of diclofenac with digoxin has been reported to increase the serum concentration and prolong the half-life of digoxin. Intervention: During concomitant use of Diclofenac Potassium and digoxin, monitor serum digoxin levels. Lithium Clinical Impact: NSAIDs have produced elevations in plasma lithium levels and reductions in renal lithium clearance. The mean minimum lithium concentration increased 15%, and the renal clearance decreased by approximately 20%. This effect has been attributed to NSAID inhibition of renal prostaglandin synthesis. Intervention: During concomitant use of Diclofenac Potassium and lithium, monitor patients for signs of lithium toxicity. Methotrexate Clinical Impact: Concomitant use of NSAIDs and methotrexate may increase the risk for methotrexate toxicity (e.g., neutropenia, thrombocytopenia, renal dysfunction). Intervention: During concomitant use of Diclofenac Potassium and methotrexate, monitor patients for methotrexate toxicity. Cyclosporine Clinical Impact: Concomitant use of Diclofenac Potassium and cyclosporine may increase cyclosporine’s nephrotoxicity. Intervention: During concomitant use of Diclofenac Potassium and cyclosporine, monitor patients for signs of worsening renal function. NSAIDs and Salicylates Clinical Impact: Concomitant use of diclofenac with other NSAIDs or salicylates (e.g., diflunisal, salsalate) increases the risk of GI toxicity, with little or no increase in efficacy [see Warnings and Precautions (5.2) ] . Intervention: The concomitant use of diclofenac with other NSAIDs or salicylates is not recommended. Pemetrexed Clinical Impact: Concomitant use of Diclofenac Potassium and pemetrexed may increase the risk of pemetrexed-associated myelosuppression, renal, and GI toxicity (see the pemetrexed prescribing information). Intervention: During concomitant use of Diclofenac Potassium and pemetrexed, in patients with renal impairment whose creatinine clearance ranges from 45 to 79 mL/min, monitor for myelosuppression, renal and GI toxicity. NSAIDs with short elimination half-lives (e.g., diclofenac, indomethacin) should be avoided for a period of two days before, the day of, and two days following administration of pemetrexed. In the absence of data regarding potential interaction between pemetrexed and NSAIDs with longer half-lives (e.g. meloxicam, nabumetone), patients taking these NSAIDs should interrupt dosing for at least five days before, the day of, and two days following pemetrexed administration. CYP2C9 Inhibitors or Inducers: Clinical Impact Diclofenac is metabolized by cytochrome P450 enzymes, predominantly by CYP2C9. Co-administration of diclofenac with CYP2C9 inhibitors (e.g., voriconazole) may enhance the exposure and toxicity of diclofenac whereas co-administration with CYP2C9 inducers (e.g. rifampin) may lead to compromised efficacy of diclofenac. Intervention: A dosage adjustment may be warranted when diclofenac is administered with CYP2C9 inhibitors or inducers [see Clinical Pharmacology (12.3) ]. Drugs that Interfere with Hemostasis (e.g. warfarin, aspirin, SSRIs/SNRIs): Monitor patients for bleeding who are concomitantly taking Diclofenac Potassium with drugs that interfere with hemostasis. Concomitant use of Diclofenac Potassium and analgesic doses of aspirin is not generally recommended (7) ACE Inhibitors, Angiotensin Receptor Blockers (ARB), or Beta-Blockers: Concomitant use with Diclofenac Potassium may diminish the antihypertensive effect of these drugs. Monitor blood pressure (7) ACE Inhibitors and ARBs: Concomitant use with Diclofenac Potassium in elderly, volume depleted, or those with renal impairment may result in deterioration of renal function. In such high risk patients, monitor for signs of worsening renal function (7) Diuretics: NSAIDs can reduce natriuretic effect of furosemide and thiazide diuretics. Monitor patients to assure diuretic efficacy including antihypertensive effects (7) Digoxin: Concomitant use with Diclofenac Potassium can increase serum concentration and prolong half-life of digoxin. Monitor serum digoxin levels (7)
How long does Diclofenac Potassium stay in your body?
The elimination half-life of diclofenac potassium is about 2 hours (terminal/elimination half-life; the label's table gives a mean of 2.3 hours in healthy adults, with wide variation between people — 48% coefficient of variation) — the time it takes the body to clear about half of it. As a rule of thumb, a medicine is mostly gone after roughly 4 to 5 half-lives, though this varies from person to person with age and kidney or liver function. This is the terminal (elimination) half-life of unchanged diclofenac, as the label labels it — "Terminal Half-life (hr) 2.3" in the PK table, and in the text "the terminal half-life of unchanged diclofenac is approximately 2 hours." Diclofenac is not a prodrug, and it has no active metabolite that outlasts it: the label names five metabolites and says the major one, 4'-hydroxy-diclofenac, has "very weak pharmacologic activity," so the parent's ~2-hour half-life is what governs. (The related diclofenac/misoprostol label notes one additional urinary metabolite with an 80-hour half-life, but it accounts for only ~1.4% of the dose.) Populations the label names: kidney impairment — no dose adjustment for mild-to-moderate impairment; in subjects with inulin clearance 60-90, 30-60 and <30 mL/min, AUC and elimination rate were comparable to healthy subjects. Liver impairment — hepatic metabolism accounts for almost 100% of diclofenac elimination, so patients with liver disease may need reduced doses; the label does not give a revised half-life number. This label reports no pharmacokinetic study in older adults or in children; the diclofenac/misoprostol label found no PK differences in subjects aged 66-81 versus younger adults. Half-life describes how the drug leaves plasma. It is not a detection window (metabolites are detectable far longer) and not dosing guidance.
This is general information, not medical advice. It doesn’t tell you when a drug test would read negative (tests detect substances for different, often longer, windows) or when it’s safe to take another dose — ask your pharmacist or prescriber. Source: DailyMed — DICLOFENAC SODIUM tablet, delayed release (FDA label, Clinical Pharmacology / Pharmacokinetics).
Drug class
How this class works, per Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) - StatPearls - NCBI Bookshelf.
May treat (source: NIH RxClass)
See how Zipsor ranks — best-rated nonsteroidal anti-inflammatory drug for:
Dosage forms
Capsule
The forms currently marketed in the U.S., per the FDA National Drug Code Directory.
Ways to save
Ask for the generic
Same active ingredient, far cheaper. Is there a generic? →
Request a 90-day supply
Bulk fills usually lower the per-dose price vs monthly refills.
Use copay cards
Manufacturer copay cards & patient-assistance programs — especially for brand drugs.
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Frequently asked questions
- What does Zipsor treat?
- Zipsor (Diclofenac Potassium) may be used to treat juvenile arthritis, rheumatoid arthritis, dysmenorrhea, inflammation, keratosis, osteoarthritis, based on NIH RxClass drug-classification data (conditions a drug may treat — not a verbatim copy of the FDA-approved label). This is general reference, not medical advice.
- How does Zipsor work?
- Zipsor is a nonsteroidal anti-inflammatory drug. NSAIDs block cyclooxygenase (COX) enzymes that your body uses to make prostaglandins, the chemicals behind pain, swelling, and fever. Lowering prostaglandins eases pain and inflammation and brings down a high temperature.
- How much does Zipsor cost?
- Nobody can tell you what you will pay — your price is set by your insurer's formulary, your deductible and the pharmacy's markup, and none of those are published. What IS published is what the pharmacy paid to acquire it: about $0.36 per ml, per the CMS NADAC survey. Treat that as the floor, not the quote — ask the pharmacist for the cash price as well as your copay, because for cheap generics the cash price often wins. Pharmacies pay less for a same-class option, Advil — about $0.04 on the same basis.
- Is there a coupon or discount for Zipsor?
- pharmaranks is an independent ratings site, not a pharmacy — we don't issue coupons or sell Zipsor. To pay less, ask your prescriber or pharmacist whether a generic equivalent exists, check the manufacturer's copay/savings card and patient-assistance program, and compare a pharmacy discount card against your insurance copay. Prices vary by pharmacy, insurance, and location, so always confirm at the counter. This is general reference, not medical or financial advice.
- Who makes Zipsor?
- Zipsor is marketed by Assertio Speclty. You can see Assertio Speclty's full profile, rating, and other products on pharmaranks.
- Is Zipsor a brand-name or generic drug?
- Zipsor is a brand-name product with the active ingredient Diclofenac Potassium. Lower-cost generic equivalents containing Diclofenac Potassium are available — ask your pharmacist.
- Is Zipsor available over the counter?
- No. Zipsor is a prescription (Rx) medication in the US — you need a prescription from a licensed clinician (in person or via telehealth); it isn't sold over the counter. For some conditions there are OTC alternatives — ask your pharmacist.
- What forms does Zipsor come in?
- Zipsor is currently marketed as capsule, per the FDA's National Drug Code Directory.
- What class of drug is Zipsor?
- Zipsor is classified as nonsteroidal anti-inflammatory drug, per the FDA's Established Pharmacologic Class.
- Is Zipsor FDA-registered?
- Zipsor is on record with the U.S. FDA under application number NDA022202. You can verify this on its official FDA label.
- Is Zipsor safe?
- There's no single safe-or-not verdict, and we don't yet have a composite recall-safety score for Zipsor. Review its FDA-label side effects and warnings below, and always consult a licensed professional.
- What are the side effects of Zipsor?
- Zipsor's side effects are taken directly from its FDA label. From the label: The following adverse reactions are discussed in greater detail in other sections of the labeling: Cardiovascular Thrombotic Events [see Warnings and Precautions (5.1) ] GI Bleeding,… Both common and serious reactions are documented in full on this page. This is general reference from the FDA, not medical advice — always consult a professional.
Clinical content sourced from the FDA label via openFDA (U.S. FDA). View the FDA label on DailyMed → Provided for general reference only — not medical advice. Always consult a licensed professional and the current prescribing information.
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