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sodium nitroprusside in 0.9% sodium chloride .2 mg/mL Injection — NDC 70436-0205-80 package photo
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sodium nitroprusside in 0.9% sodium chloride .2 mg/mL Injection — NDC 70436-205-80 (Billing 70436-0205-80)

by Slate Run Pharmaceuticals, LLC · 1 VIAL, SINGLE-DOSE in 1 CARTON / 50 mL in 1 VIAL, SINGLE-DOSE

This is a package of sodium nitroprusside in 0.9% sodium chloride .2 mg/mL Injection from Slate Run Pharmaceuticals, LLC, marketed since Dec 2022 and currently FDA-listed. It is this product's only package size.

NDC 70436-0205-80
🏷️ FDA NDC (as labeled) 70436-205-80 billing pads the product segment with a zero
Rx only Generic On market Non-controlled ⇄ Compare with another NDC
🗂️ FDA directory synced Oct 1, 2026 · this listing last changed Jul 24, 2026 · sources: openFDA · FDA label (DailyMed) · FDA Orange & Purple Book · First Databank · CMS NADAC, ASP, Medicare & Medicaid · RxNorm
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Compiled from public FDA, CMS, DailyMed, NADAC, and related drug data sources. Editorial policy

Identity & classification

Regulatory identifiers FDA, NLM and CMS codes for this package

FDA NDC (as labeled) 70436-205-80
Product NDC 70436-205
11-digit billing NDC 70436020580
RxCUI 1876368, 1999185, 2052423
UNII EAO03PE1TC
UPC 0370436206803
Application # ANDA215846
SPL Set ID 6f02e4ac-5f7c-4003-b9b7-283f489cddb0
Established class (EPC) Vasodilator
Physiologic effect Vasodilation
DEA schedule Non-controlled
Marketing category ANDA
Marketing status On market
FDA listing status Listed (active directory)
Marketing start 2022-12-31
Route INTRAVENOUS
Dosage form INJECTION
Substance SODIUM NITROPRUSSIDE
Quick answers
  • RxCUI (RxNorm): 1876368
Why two NDCs? The FDA registers this code as 70436-205-80 — a 5-3-2 layout, and that's what's printed on the package and shown on DailyMed. For insurance claims, every NDC is standardized to a uniform 11-digit 5-4-2 format by adding a zero to the product segment → 70436-0205-80. Same drug, same package — only the format differs.
Where does this data come from?
Identifiers from the FDA openFDA NDC Directory and Structured Product Labeling; RxCUI from RxNorm (NLM); GPI from Medi-Span; GCN / HIC / AHFS / legend from First Databank.

RxNorm drug class

This medicine belongs to the Vasodilator class.

Pharmacologic class Vasodilator
Drug family (ATC) Nitroferricyanide derivatives
Where does this data come from?
Therapeutic classes from RxNorm RxClass (U.S. National Library of Medicine) — Established Pharmacologic Class (FDA), ATC drug family (WHO) and mechanism of action, matched by this product’s RxCUI.

Clinical

Supplement & herbal interactions

🌿 Drug–supplement interaction checker →
Where does this data come from?
Plain-language summary from MedlinePlus (U.S. National Library of Medicine); supplement & herbal interactions and nutrient depletion data from the Natural Medicines database; our full guide is HelloPharmacist editorial content.

Pricing

A drug doesn't have one price. Each row is a different public payment system, and none is what you'd pay at the counter — that depends on your insurance. The ⓘ on each row explains what it measures.

Price systemPer eachPer package
Retail pharmacies payNADAC · weekly Not in the retail survey — common for institutional, discontinued, or low-volume packs.
Medicaid paysCMS SDUD · 12 mo No recent Medicaid claims on file for this NDC — rare and low-volume NDCs are suppressed in the public data.
Medicare drug plans payPart D · quarterly No Part D plan price is available for this NDC in our data.
ℹ️
No price is published for this exact package yet. CMS surveys NADAC per package size, so a different pack of the same drug often has one.
Where does this data come from?
NADAC (National Average Drug Acquisition Cost) is the CMS weekly pharmacy-acquisition-cost survey — what pharmacies pay. ASP (Average Sales Price) is the CMS Medicare Part B drug-payment file, published quarterly. Medicaid pays is computed by us from CMS State Drug Utilization Data (total reimbursed ÷ units, trailing 12 months) — gross of rebates and inclusive of dispensing fees, so it reflects what Medicaid paid, not an acquisition cost. Medicare drug plans pay is the median negotiated point-of-sale unit cost across plans listing this NDC in the CMS quarterly Prescription Drug Plan pricing files, before rebates. The VA pays is the federal contract price (FSS, and the statutory Big 4 ceiling where listed) from the VA National Acquisition Center pharmaceutical price file. All are free public government data; each measures a different payer, so the figures are not directly comparable.

Packaging — all sizes for this product

Package NDCDescription Marketing startMarketing endStatus
70436-0205-80 You're viewing this Main listing 1 VIAL, SINGLE-DOSE in 1 CARTON / 50 mL in 1 VIAL, SINGLE-DOSE 2022-12-31 — Active

Therapeutic equivalents

ProductLabelerPackNADAC/unitTEStatusPrice vs. this
Sodium Nitroprusside .2 mg/mL 14335-0132-01 Hainan 1 vial — — FDA listed —
sodium nitroprusside in 0.9% sodium chloride .2 mg/mLthis 70436-0205-80 Slate 1 vial — — FDA listed —
sodium nitroprusside in 0.9% sodium chloride .2 mg/mL 70436-0206-80 Slate 1 vial — — FDA listed —
About this product: this is a generic version of the medicine. FDA equivalence ratings are shown when available, and other versions are listed above, least expensive first.
Where does this data come from?
Equivalents are other NDCs of the same ingredient, form and route from the openFDA NDC Directory, ranked least-expensive-first by NADAC. Therapeutic-equivalence (AB) ratings come from the FDA Orange Book; biologics use the FDA Purple Book for biosimilar & interchangeable status.

Availability & generic status

🏛️
2022
On the market since
Dec 2022
📍
2026
Currently FDA-listed
4 years listed
🔓
·
Generic on the market
this product is a generic
✅This is a generic drug

This product is an FDA-approved generic. Other versions of the same drug are listed under Therapeutic equivalents, least expensive first.

Where does this data come from?
Patents and exclusivity from the FDA Orange Book (small-molecule drugs), refreshed from public FDA data. Generic launch timing is an estimate, not a guarantee.

Inactive Ingredients / Excipients

Inactive ingredients, also called excipients, are components of the drug product other than the active ingredient. They may include fillers, dyes, coatings, preservatives, flavors, or other formulation ingredients.

Loading inactive ingredients from the official FDA label in the background. No external source is being called by this page request.
Where does this data come from?
Source: official FDA Structured Product Labeling (SPL) via DailyMed and the openFDA label index. Structured IACT rows and label-wide narrative are kept separate; availability and product-level specificity depend on the submitted label.

Inactive ingredient FAQ

Are inactive ingredients the same for every manufacturer?
No. Inactive ingredients can differ by manufacturer, dosage form, strength, and package / product version.
Why might an inactive ingredient be missing?
Some SPLs do not provide a complete structured inactive-ingredient list, and older or unusual labels may only include the information in narrative text.
Can inactive ingredients matter?
Yes. They can matter for allergies, intolerances, dyes, gluten / lactose concerns, preservatives, and formulation differences — but confirm with a pharmacist or the manufacturer when it’s clinically important.

Manufacturer & labeler

LabelerSlate Run Pharmaceuticals, LLC
Application holderHAINAN POLY PHARM CO LTD
FDA applicationANDA215846 (ANDA)
Labeler code70436
First marketedDec 2022
Product typeHuman Prescription Drug
Portfolio109 products on file
The labeler markets the product; the application holder owns the FDA approval. They’re often the same company but can differ (e.g. a repackager or an authorized generic). A mailing address / phone appears here when the manufacturer includes it in the product’s FDA label (not all do).
Where does this data come from?
Labeler, application holder and registered establishment from the FDA openFDA NDC Directory and Drugs@FDA; address/contact from the product’s FDA label.

Full prescribing information FDA SPL

The complete FDA label for this product — the official prescribing information, verbatim, section by section. Very long sections are excerpted here and marked; the full text is on DailyMed (linked in the sources below). Jump with a chip, search within the label, or expand everything.
🚨 Boxed Warning 🎯 Indications and Usage ⏱️ Dosage and Administration 💊 Dosage Forms and Strengths ⛔ Contraindications ⚠️ Warnings and Cautions 🤒 Adverse Reactions 👥 Use in Specific Populations 🤰 Pregnancy 🧒 Pediatric Use 🆘 Overdosage 🧬 Clinical Pharmacology 🧬 Mechanism of Action 📦 How Supplied / Storage and Handling 📋 Description 💬 Information for Patients 🧬 Pharmacokinetics 🧬 Pharmacodynamics 🔬 Clinical Studies 🧪 Nonclinical Toxicology 📄 Carcinogenesis, Mutagenesis, Impairment of Fertility 📄 Package Label / Principal Display Panel
🚨 Boxed Warning 201 words ▾

WARNING: (A) EXCESSIVE HYPOTENSION; (B) CYANIDE TOXICITY (A) EXCESSIVE HYPOTENSION: Sodium nitroprusside can cause precipitous decreases in blood pressure which can lead to irreversible ischemic injuries or death. Use only with continuous blood pressure monitoring [see Dosage and Administration ( 2.2 ) and Warnings and Precautions ( 5.1 ) ] . (B) CYANIDE TOXICITY: Sodium nitroprusside metabolism produces dose-related cyanide, which can be lethal.

A patient’s ability to buffer cyanide will be exceeded in less than one hour at the maximum dose rate (10 mcg/kg/min); limit infusion at the maximum rate to as short a duration as possible [see Warnings and Precautions ( 5.2 ) ] . WARNING: (A) EXCESSIVE HYPOTENSION; (B) CYANIDE TOXICITY See full prescribing information for complete boxed warning. (A) Sodium Nitroprusside can cause precipitous decreases in blood pressure which can lead to irreversible ischemic injuries or death.

Use only with continuous blood pressure monitoring. ( 2.2 , 5.1 ) (B) Sodium nitroprusside metabolism produces dose-related cyanide, which can be lethal. A patient’s ability to buffer cyanide will be exceeded in less than one hour at the maximum dose rate (10 mcg/kg/min); limit infusion at the maximum rate to as short a duration as possible ( 5.2 ).

🎯 Indications and Usage 144 words ▾

1 INDICATIONS AND USAGE Sodium nitroprusside is a direct acting vasodilator indicated for: Immediate reduction of blood pressure ( 1.1 ) Producing controlled hypotension to reduce bleeding during surgery ( 1.2 ) Treatment of acute heart failure to reduce left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, peripheral vascular resistance and mean arterial blood pressure ( 1.3 )

1.1Immediate Reduction of Blood Pressure Sodium nitroprusside is indicated for the immediate reduction of blood pressure of adult and pediatric patients in hypertensive crises.

1.2Induction and Maintenance of Controlled Hypotension Sodium nitroprusside indicated for induction and maintenance of controlled hypotension in adults and children during surgery, to reduce bleeding.

1.3Treatment of Acute Heart Failure Sodium nitroprusside is indicated for the treatment of acute heart failure to reduce left ventricular end-diastolic pressure, pulmonary capillary wedge pressure, peripheral vascular resistance and mean arterial blood pressure.

⏱️ Dosage and Administration ~1 min read ▾

2 DOSAGE AND ADMINISTRATION Initiate infusion of sodium nitroprusside at a rate of 0.3 mcg/kg/min, and titrate every few minutes until the desired effect is achieved OR the maximum recommended infusion rate of 10 mcg/kg/min has been reached ( 2.2 ).

2.1Inspection Inspect parenteral drug products for particulate matter and discoloration prior to administration, whenever solution and container permit. Sodium nitroprusside should be a clear colorless to red/brown color; do not use if solution is blue, green, or bright red. Dosing Continuously monitor blood pressure in patients receiving sodium nitroprusside.

Start infusion of sodium nitroprusside at a rate of 0.3 mcg/kg/min. Evaluate blood pressure for at least 5 minutes before titrating to a higher or lower dose to achieve the desired blood pressure. The dose may be titrated upward until: the desired effect is achieved, systemic blood pressure cannot be further reduced without compromising the perfusion of vital organs, or the maximum recommended infusion rate of 10 mcg/kg/min has been reached, whichever occurs first.

In patients with eGFR <30 mL/min/1.73 m 2 , limit the mean infusion rate to less than 3 mcg/kg/min. In anuric patients, limit the mean infusion rate to 1 mcg/kg/min.

2.3Administration Do not administer other drugs in the same solution with sodium nitroprusside. Sodium nitroprusside must be delivered by a volumetric infusion pump because small variations in infusion rate can lead to wide, undesirable variations in blood pressure [see Clinical Pharmacology ( 12.2 )].

💊 Dosage Forms and Strengths 121 words ▾

3 DOSAGE FORMS AND STRENGTHS Injection: 50 mg/100 mL of 0.9% sodium chloride (0.5 mg/mL), 20 mg/100 mL of 0.9% sodium chloride (0.2 mg/mL), and 10 mg/50 mL of 0.9% sodium chloride (0.2 mg/mL). Sodium Nitroprusside in 0.9% Sodium Chloride Injection, ready to use is supplied as a sterile, unpreserved, colorless to red-brown solution available in a single-dose vial. Injection: 50 mg of sodium nitroprusside in 100 mL of 0.9% sodium chloride (0.5 mg/mL) in 100 mL single-dose vials, 20 mg of sodium nitroprusside in 100 mL of 0.9% sodium chloride (0.2 mg/mL) in 100 mL single-dose vials and 10 mg of sodium nitroprusside in 50 mL of 0.9% sodium chloride (0.2 mg/mL) in 50 mL single-dose vials ( 3 ).

⛔ Contraindications 116 words ▾

4 CONTRAINDICATIONS Diseases with compensatory hypertension (e.g., coarctation of the aorta, arteriovenous shunting). Inadequate cerebral circulation or in moribund patients (A.S.A. Class 5E) coming to emergency surgery.

Patients with congenital (Leber’s) optic atrophy or with tobacco amblyopia. Acute heart failure associated with reduced peripheral vascular resistance. Concomitant use with sildenafil, tadalafil, vardenafil, or riociguat.

Diseases with compensatory hypertension (e.g. coarctation of the aorta, arteriovenous shunting) ( 4 ). Inadequate cerebral circulation or moribund patients (A.S.A. Class 5E) coming to emergency surgery ( 4 ).

Congenital (Leber’s) optic atrophy or tobacco amblyopia ( 4 ). Acute heart failure with reduced peripheral vascular resistance ( 4 ). Concomitant use with sildenafil, tadalafil, vardenafil, or riociguat ( 4 ).

⚠️ Warnings and Cautions ~2 min read ▾

5 WARNINGS AND PRECAUTIONS Thiocynate toxicity ( 5.3 ) Methemoglobinemia ( 5.4 ) Increases in intracranial pressure ( 5.5 ) Diminished capacity to compensate for anemia and hypovolemia with anesthesia during surgery ( 5.6 )

5.1Excessive Hypotension Sodium nitroprusside, can cause excessive hypotension leading to hypoperfusion of vital organs. Hypotension should resolve within 1-10 minutes after discontinuation of the nitroprusside infusion; during these few minutes, it may be helpful to put the patient into a head-down (Trendelenburg) position to maximize venous return. If hypotension persists more than a few minutes after discontinuation, consider other causes.

Elderly patients may be more sensitive to the hypotensive effects of the drug.

5.2Cyanide Toxicity Sodium nitroprusside infusions above 2 mcg/kg/min generate cyanide ion (CN¯) faster than the body can normally dispose of it. At the maximum recommended infusion rate of 10 mcg/kg/min, the patient’s ability to buffer CN¯ will be exceeded in less than one hour [see Overdose ( 10 )] . Patients with hepatic dysfunction are more susceptible to cyanide toxicity.

An early manifestation of cyanide toxicity is increasing dosage requirements to maintain blood pressure control. Metabolic acidosis may not be evident for more than an hour after toxic cyanide levels accumulate. If cyanide toxicity develops, discontinue sodium nitroprusside, and consider specific treatment of cyanide toxicity [see Overdosage ( 10 )].

5.3Thiocyanate Toxicity Most of the cyanide produced during metabolism of sodium nitroprusside is eliminated in the form of thiocyanate. Thiocyanate is mildly neurotoxic (tinnitus, miosis, hyperreflexia) at serum levels of 1 mmol/L (60 mg/L). Thiocyanate is life-threatening when levels reach ~200 mg/L.

Therefore, routine monitoring of plasma thiocyanate levels is recommended in patients with normal renal function when cumulative sodium nitroprusside doses exceed 7 mg/kg/day. In patients with eGFR <30 mL/min/1.73 m 2 , limit the mean infusion rate to less than 3 mcg/kg/min. In anuric patients, limit the mean infusion rate to 1 mcg/kg/min.

Renal hemodialysis may be used to eliminate thiocyanate in cases of severe toxicity.

5.4Methemoglobinemia Sodium nitroprusside infusions cause conversion of hemoglobin to methemoglobin in a dose- dependent manner. Methemoglobin binds oxygen more strongly than does hemoglobin, and when methemoglobin levels are elevated, oxygen release from red blood cells in tissue capillaries may be impaired. However, conversion of methemoglobin back to hemoglobin is normally rapid, and clinically significant methemoglobinemia is infrequent.

Suspect methemoglobinemia in patients who have received >10 mg/kg of sodium nitroprusside and who exhibit signs of impaired oxygen delivery despite adequate cardiac output and adequate arterial pO2. Methemoglobinemic blood is chocolate brown, without the expected color change on exposure to air. Methemoglobin levels >10% are considered clinically significant.

When methemoglobinemia is diagnosed, the treatment of choice is 1-2 mg/kg of methylene blue, administered intravenously over several minutes.

5.5Increased Intracranial Pressure Like other vasodilators, sodium nitroprusside can cause increases in intracranial pressure.

5.6Anemia and Hypovolemia with Anesthesia When sodium nitroprusside (or any other vasodilator) is used for controlled hypotension during anesthesia, the patient’s capacity to compensate for anemia and hypovolemia may be diminished. If possible, correct pre-existing anemia and hypovolemia prior to administration.

🤒 Adverse Reactions 146 words ▾

6 ADVERSE REACTIONS The following adverse reactions are described, or described in greater detail, in other sections: Hypotension [see Warnings and Precautions ( 5.1 )] Cyanide Toxicity [see Warnings and Precautions ( 5.2 )] Thiocyanate Toxicity [see Warnings and Precautions ( 5.3 )] Methemoglobinemia [see Warnings and Precautions ( 5.4 )] Increased Intracranial Pressure [see Warnings and Precautions ( 5.5 )] Anemia and Hypovolemia [see Warnings and Precautions ( 5.6 )] Less common adverse reactions include: Cardiovascular: Bradycardia, electrocardiographic changes, tachycardia, palpitations, retrosternal discomfort Dermatologic: Rash Endocrine: Hypothyroidism Gastrointestinal: Ileus, nausea, abdominal pain Hematologic: Decreased platelet aggregation Musculoskeletal: Muscle twitching Neurologic: Increased intracranial pressure, dizziness, headache Miscellaneous: Flushing, diaphoresis, venous streaking, irritation at the infusion site Most common adverse reactions are hypotension and cyanide toxicity ( 6 ).

To report SUSPECTED ADVERSE REACTIONS, contact Slate Run Pharmaceuticals, LLC at 1-888-341-9214 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

👥 Use in Specific Populations ~2 min read ▾

8 USE IN SPECIFIC POPULATIONS

8.1Pregnancy Risk Summary Based on animal data and mechanism of action, sodium nitroprusside may lead to cyanide exposure and potential adverse effects in the fetus [see Clinical Pharmacology ( 12.3 ) and Clinical Considerations ] . Published post-marketing reports with sodium nitroprusside use in pregnant women are insufficient to inform a drug-associated risk of adverse pregnancy related outcomes [see Data ] . There were no animal reproduction studies conducted with sodium nitroprusside during pregnancy.

However, there are published studies in pregnant sheep that demonstrate that nitroprusside crosses the placenta and that fetal cyanide levels were dose-related to maternal levels of sodium nitroprusside [see Data]. Advise pregnant women of the potential risk to a fetus. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. Clinical Considerations Fetal/Neonatal Adverse Reactions Prolonged use and large doses of sodium nitroprusside during pregnancy may result in cyanide toxicity that may be fatal to the fetus.

In the unusual case that there is no appropriate alternative to therapy with sodium nitroprusside for a particular patient, apprise the mother of the potential risk to the fetus [see Warnings and Precautions ( 5.2 )] . Data Human Data A small number of cases have reported adverse events, including stillbirths, in pregnant women with severe pregnancy-induced hypertension who were treated with sodium nitroprusside. However, methodological limitations, including small sample size and limited information on sodium nitroprusside dosage and duration of treatment, as well as the cyanide concentration in maternal blood or fetal tissue, preclude a reliable evaluation of the potential risk of adverse fetal outcomes with the use of sodium nitroprusside during pregnancy.

Animal Data In three studies in pregnant ewes, nitroprusside was shown to cross the placental barrier. Fetal cyanide levels were shown to be dose-related to maternal levels of nitroprusside. The metabolic transformation of sodium nitroprusside given to pregnant ewes led to fatal levels of cyanide in the fetuses.

The infusion of 25 mcg/kg/min of sodium nitroprusside for one hour in pregnant ewes resulted in the death of all fetuses. Pregnant ewes infused with 1 mcg/kg/min of sodium nitroprusside for one hour delivered normal lambs.

8.2Lactation Risk Summary There is no information about the presence of sodium nitroprusside in human milk, the effects on the breastfed infant, or the effects on milk production. Thiocyanate, one of sodium nitroprusside’s metabolites, is present in human milk. It is unclear how long, if ever, levels of thiocyanate in milk are clinically relevant.

8.4Pediatric Use Efficacy in the pediatric population was established based on adult trials and supported by the dose-ranging trial (Study 1) and an open label trial of at least 12 hour infusion at a rate that achieved adequate MAP control (Study 2) with pediatric patients on sodium nitroprusside. No novel safety issues were seen in these studies in pediatric patients [see Clinical Studies ( 14 )].

🤰 Pregnancy ~2 min read ▾

8.1Pregnancy Risk Summary Based on animal data and mechanism of action, sodium nitroprusside may lead to cyanide exposure and potential adverse effects in the fetus [see Clinical Pharmacology ( 12.3 ) and Clinical Considerations ] . Published post-marketing reports with sodium nitroprusside use in pregnant women are insufficient to inform a drug-associated risk of adverse pregnancy related outcomes [see Data ] . There were no animal reproduction studies conducted with sodium nitroprusside during pregnancy.

However, there are published studies in pregnant sheep that demonstrate that nitroprusside crosses the placenta and that fetal cyanide levels were dose-related to maternal levels of sodium nitroprusside [see Data]. Advise pregnant women of the potential risk to a fetus. The estimated background risk of major birth defects and miscarriage for the indicated population is unknown.

All pregnancies have a background risk of birth defect, loss, or other adverse outcomes. In the U.S. general population, the estimated background risk of major birth defects and miscarriage in clinically recognized pregnancies is 2-4% and 15-20%, respectively. Clinical Considerations Fetal/Neonatal Adverse Reactions Prolonged use and large doses of sodium nitroprusside during pregnancy may result in cyanide toxicity that may be fatal to the fetus.

In the unusual case that there is no appropriate alternative to therapy with sodium nitroprusside for a particular patient, apprise the mother of the potential risk to the fetus [see Warnings and Precautions ( 5.2 )] . Data Human Data A small number of cases have reported adverse events, including stillbirths, in pregnant women with severe pregnancy-induced hypertension who were treated with sodium nitroprusside. However, methodological limitations, including small sample size and limited information on sodium nitroprusside dosage and duration of treatment, as well as the cyanide concentration in maternal blood or fetal tissue, preclude a reliable evaluation of the potential risk of adverse fetal outcomes with the use of sodium nitroprusside during pregnancy.

Animal Data In three studies in pregnant ewes, nitroprusside was shown to cross the placental barrier. Fetal cyanide levels were shown to be dose-related to maternal levels of nitroprusside. The metabolic transformation of sodium nitroprusside given to pregnant ewes led to fatal levels of cyanide in the fetuses.

The infusion of 25 mcg/kg/min of sodium nitroprusside for one hour in pregnant ewes resulted in the death of all fetuses. Pregnant ewes infused with 1 mcg/kg/min of sodium nitroprusside for one hour delivered normal lambs.

🧒 Pediatric Use 67 words ▾

8.4Pediatric Use Efficacy in the pediatric population was established based on adult trials and supported by the dose-ranging trial (Study 1) and an open label trial of at least 12 hour infusion at a rate that achieved adequate MAP control (Study 2) with pediatric patients on sodium nitroprusside. No novel safety issues were seen in these studies in pediatric patients [see Clinical Studies ( 14 )].

🆘 Overdosage ~1 min read ▾

10 OVERDOSAGE Overdosage of nitroprusside can be manifested as excessive hypotension or cyanide toxicity [see Warnings and Precaution ( 5.1 , 5.2 )] or as thiocyanate toxicity [see Warnings and Precautions ( 5.3 )] . Cyanide toxicity causes venous hyperoxemia with bright red venous blood. Cells become unable to extract the oxygen delivered to them, leading to air hunger, confusion and death.

Lactic acidosis may occur, but its emergence may lag other life-threatening manifestations of cyanide toxicity. Cyanide levels can be measured by many laboratories, and blood-gas studies that can detect venous hyperoxemia or acidosis are widely available. Acidosis may not appear until more than an hour after the appearance of dangerous cyanide levels.

Suspicion of cyanide toxicity is adequate grounds for initiation of treatment. Treatment of cyanide toxicity consists of: discontinuing sodium nitroprusside; administration of sodium nitrite to convert as much hemoglobin into methemoglobin as the patient can safely tolerate; and then infusing sodium thiosulfate to convert the cyanide into thiocyanate Hemodialysis is ineffective in removal of cyanide, but it will eliminate most thiocyanate. Sodium nitrite is available in a 3% solution, and 4-6 mg/kg (about 0.2 mL/kg) should be injected over 2-4 minutes.

This dose can be expected to convert about 10% of the patient’s hemoglobin into methemoglobin; this level of methemoglobinemia is not associated with any important hazard of its own. Immediately after infusion of the sodium nitrite, sodium thiosulfate should be infused. This agent is available in 10% and 25% solutions, and the recommended dose is 150-200 mg/kg; a typical adult dose is 50 mL of the 25% solution.

Thiosulfate treatment of an acutely cyanide-toxic patient will raise thiocyanate levels, but not to a dangerous degree. The nitrite/thiosulfate regimen may be repeated, at half the original doses, after two hours. Cyanide antidote kits are available.

🧬 Clinical Pharmacology ~3 min read ▾

12 CLINICAL PHARMACOLOGY

12.1Mechanism of Action Sodium nitroprusside interacts with oxyhemoglobin to produce methemoglobin, cyanide, and nitric oxide (NO). NO then reacts with guanylate cyclase in vascular smooth muscle to produce cGMP that reduces intracellular calcium concentrations resulting in relaxation of vascular smooth muscle and consequent dilatation of peripheral arteries and veins. Other smooth muscle (e.g., uterus, duodenum) is not affected.

Sodium nitroprusside is more active on veins than on arteries, but this selectivity is much less marked than that of nitroglycerin. Dilatation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure (afterload).

Dilatation of the coronary arteries also occurs.

12.2Pharmacodynamics In association with the decrease in blood pressure, sodium nitroprusside administered intravenously to hypertensive and normotensive patients produces slight increases in heart rate and a variable effect on cardiac output. In hypertensive patients, moderate doses induce renal vasodilatation roughly proportional to the decrease in systemic blood pressure, so there is no appreciable change in renal blood flow or glomerular filtration rate. The hypotensive effect of sodium nitroprusside is seen within a minute or two after the start of an adequate infusion, and it dissipates almost as rapidly after an infusion is discontinued.

The effect is augmented by ganglionic blocking agents and inhaled anesthetics.

12.3Pharmacokinetics Infused sodium nitroprusside is rapidly distributed to a volume that is approximately coextensive with the extracellular space. The drug is cleared by intraerythrocytic reaction with hemoglobin (Hgb), and sodium nitroprusside’s resulting circulatory half-life is about 2 minutes. The products of the nitroprusside/hemoglobin reaction are cyanmethemoglobin (cyanmetHgb) and cyanide ion (CN¯).

Metabolism As shown in the diagram below, the essential features of nitroprusside metabolism are: one molecule of sodium nitroprusside is metabolized by combination with hemoglobin to produce one molecule of cyanmethemoglobin and four CN¯ ions; methemoglobin, obtained from hemoglobin, can sequester cyanide as cyanmethemoglobin; thiosulfate reacts with cyanide to produce thiocyanate; thiocyanate is eliminated in the urine; cyanide not otherwise removed binds to cytochromes; and cyanide is much more toxic than methemoglobin or thiocyanate.

Cyanide ion is normally found in serum; it is derived from dietary substrates and from tobacco smoke. CN¯ levels in packed erythrocytes are typically less than 1 μmol/L (less than 25 mcg/L); levels are roughly doubled in heavy smokers. At healthy steady state, most people have less than 1% of their hemoglobin in the form of methemoglobin.

Nitroprusside metabolism can lead to methemoglobin formation. Relatively large quantities of sodium nitroprusside, however, are required to produce significant methemoglobinemia. At physiologic methemoglobin levels, the CN¯ binding capacity of packed red cells is a little less than 200 μmol/L (5 mg/L).

Cytochrome toxicity is seen at levels only slightly higher, and death has been reported at levels from 300 to 3000 μmol/L (8–80 mg/L). A patient with a normal redcell mass (35 mL/kg) and normal methemoglobin levels can buffer about 175 mcg/kg of CN¯, corresponding to a little less than 500 mcg/kg of infused sodium nitroprusside. Thiocyanate (SCN¯) is a normal physiological constituent of serum, with normal levels typically in the range of 50-250 μmol/L (3-15 mg/L).

Clearance of SCN¯ is primarily renal. In renal failure, the half-life can be doubled or tripled. When thiosulfate is being supplied only by normal physiologic mechanisms, conversion of CN¯ to SCN¯ generally proceeds… [Excerpted — this section continues on DailyMed.]

🧬 Mechanism of Action 130 words ▾

12.1Mechanism of Action Sodium nitroprusside interacts with oxyhemoglobin to produce methemoglobin, cyanide, and nitric oxide (NO). NO then reacts with guanylate cyclase in vascular smooth muscle to produce cGMP that reduces intracellular calcium concentrations resulting in relaxation of vascular smooth muscle and consequent dilatation of peripheral arteries and veins. Other smooth muscle (e.g., uterus, duodenum) is not affected.

Sodium nitroprusside is more active on veins than on arteries, but this selectivity is much less marked than that of nitroglycerin. Dilatation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure (afterload).

Dilatation of the coronary arteries also occurs.

📦 How Supplied / Storage and Handling 84 words ▾

16 HOW SUPPLIED/STORAGE AND HANDLING Sodium Nitroprusside in 0.9% Sodium Chloride Injection, ready to use is supplied in amber-colored, single-dose, 50 mg/100 mL (0.5 mg/mL) Fliptop Vials (NDC 70436-207-80), 20 mg/100 mL (0.2 mg/mL) Fliptop Vials (NDC 70436-206-80) and 10 mg/50 mL (0.2 mg/mL) Fliptop Vials (NDC 70436-205-80). Store at 20° to 25°C (68° to 77°F). [See USP Controlled Room Temperature]. To protect Sodium Nitroprusside in 0.9% Sodium Chloride Injection, ready to use from light, vial should be stored in its carton until used.

📋 Description ~1 min read ▾

11 DESCRIPTION Sodium nitroprusside is disodium pentacyanonitrosylferrate (2-) dihydrate, a hypotensive agent whose structural formula is Sodium Nitroprusside has a molecular formula Na 2 [Fe(CN) 5 NO] • 2H 2 O and molecular weight of 297.95. Dry sodium nitroprusside is a reddish-brown powder, soluble in water. Sodium nitroprusside solution is rapidly degraded by trace contaminants, often with resulting color changes [see Dosage and Administration ( 2.1 )].

Sodium Nitroprusside in 0.9% Sodium Chloride Injection, ready to use is supplied as a sterile, unpreserved, colorless to red-brown solution packaged in a single-dose 100-mL vial. Each 100 mL of solution in vial contains 50 mg of sodium nitroprusside (0.5 mg/mL), 900 mg of sodium chloride, USP (9 mg/mL), in sterile water for injection, USP. Sodium Nitroprusside in 0.9% Sodium Chloride Injection, ready to use is also supplied as a sterile, unpreserved, colorless to red-brown solution packaged in a single-dose 100-mL vial.

Each 100 mL of solution in vial contains 20 mg of sodium nitroprusside (0.2 mg/mL), 900 mg of sodium chloride, USP (9 mg/mL), in sterile water for injection, USP. Sodium Nitroprusside in 0.9% Sodium Chloride Injection, ready to use is also supplied as a sterile, unpreserved, colorless to red-brown solution packaged in a single-dose 50-mL vial. Each 50 mL of solution in vial contains 10 mg of sodium nitroprusside (0.2 mg/mL), 450 mg of sodium chloride, USP (9 mg/mL), in sterile water for injection, USP. chemical structure

💬 Information for Patients 65 words ▾

17 PATIENT COUNSELING INFORMATION Pregnancy Inform female patients of reproductive potential that Sodium Nitroprusside Injection may cause fetal harm and to inform their prescriber of a known or suspected pregnancy [see Use in Specific Population ( 8.1 )]. Manufactured by: Hainan Poly Pharm. Co., Ltd., Guilinyang Economic Development Zone, Haikou, Hainan, China 571127 Distributed by: Slate Run Pharmaceuticals, LLC, Columbus, Ohio 43215 10000403/01 Revised 02/2023

🧬 Pharmacokinetics ~2 min read ▾

12.3Pharmacokinetics Infused sodium nitroprusside is rapidly distributed to a volume that is approximately coextensive with the extracellular space. The drug is cleared by intraerythrocytic reaction with hemoglobin (Hgb), and sodium nitroprusside’s resulting circulatory half-life is about 2 minutes. The products of the nitroprusside/hemoglobin reaction are cyanmethemoglobin (cyanmetHgb) and cyanide ion (CN¯).

Metabolism As shown in the diagram below, the essential features of nitroprusside metabolism are: one molecule of sodium nitroprusside is metabolized by combination with hemoglobin to produce one molecule of cyanmethemoglobin and four CN¯ ions; methemoglobin, obtained from hemoglobin, can sequester cyanide as cyanmethemoglobin; thiosulfate reacts with cyanide to produce thiocyanate; thiocyanate is eliminated in the urine; cyanide not otherwise removed binds to cytochromes; and cyanide is much more toxic than methemoglobin or thiocyanate.

Cyanide ion is normally found in serum; it is derived from dietary substrates and from tobacco smoke. CN¯ levels in packed erythrocytes are typically less than 1 μmol/L (less than 25 mcg/L); levels are roughly doubled in heavy smokers. At healthy steady state, most people have less than 1% of their hemoglobin in the form of methemoglobin.

Nitroprusside metabolism can lead to methemoglobin formation. Relatively large quantities of sodium nitroprusside, however, are required to produce significant methemoglobinemia. At physiologic methemoglobin levels, the CN¯ binding capacity of packed red cells is a little less than 200 μmol/L (5 mg/L).

Cytochrome toxicity is seen at levels only slightly higher, and death has been reported at levels from 300 to 3000 μmol/L (8–80 mg/L). A patient with a normal redcell mass (35 mL/kg) and normal methemoglobin levels can buffer about 175 mcg/kg of CN¯, corresponding to a little less than 500 mcg/kg of infused sodium nitroprusside. Thiocyanate (SCN¯) is a normal physiological constituent of serum, with normal levels typically in the range of 50-250 μmol/L (3-15 mg/L).

Clearance of SCN¯ is primarily renal. In renal failure, the half-life can be doubled or tripled. When thiosulfate is being supplied only by normal physiologic mechanisms, conversion of CN¯ to SCN¯ generally proceeds at about 1 mcg/kg/min.

This rate of CN¯ clearance corresponds to steady-state processing of a sodium nitroprusside infusion of slightly more than 2 mcg/kg/min. CN¯ begins to accumulate when sodium nitroprusside infusions exceed this rate. metabolism of sodium nitroprusside

🧬 Pharmacodynamics 105 words ▾

12.2Pharmacodynamics In association with the decrease in blood pressure, sodium nitroprusside administered intravenously to hypertensive and normotensive patients produces slight increases in heart rate and a variable effect on cardiac output. In hypertensive patients, moderate doses induce renal vasodilatation roughly proportional to the decrease in systemic blood pressure, so there is no appreciable change in renal blood flow or glomerular filtration rate. The hypotensive effect of sodium nitroprusside is seen within a minute or two after the start of an adequate infusion, and it dissipates almost as rapidly after an infusion is discontinued.

The effect is augmented by ganglionic blocking agents and inhaled anesthetics.

🔬 Clinical Studies ~2 min read ▾

14 CLINICAL STUDIES Baseline-controlled clinical trials have uniformly shown that sodium nitroprusside has a prompt hypotensive effect, at least initially, in all populations. With increasing rates of infusion, sodium nitroprusside has been able to lower blood pressure without an observed limit of effect. Clinical trials have also shown that the hypotensive effect of sodium nitroprusside is associated with reduced blood loss in a variety of major surgical procedures.

In patients with acute heart failure and increased peripheral vascular resistance, administration of sodium nitroprusside causes reductions in peripheral resistance, increases in cardiac output, and reductions in left ventricular filling pressure. Progressive tachyphylaxis to the hypotensive effects of sodium nitroprusside has been reported in several trials and numerous case reports. The mechanism of tachyphylaxis to sodium nitroprusside remains unknown.

Pediatric The effects of sodium nitroprusside to induce hypotension were evaluated in two trials in pediatric patients less than 17 years of age. In both trials, at least 50% of the patients were pre-pubertal, and about 50% of these pre-pubertal patients were less than 2 years of age, including 4 neonates. The primary efficacy variable was the mean arterial pressure (MAP).

There were 203 pediatric patients in a parallel, dose-ranging study (Study 1). During the 30-minute blinded phase, patients were randomized 1:1:1:1 to receive sodium nitroprusside 0.3, 1, 2, or 3 mcg/kg/min. The infusion rate was increased step-wise to the target dose rate (i.e., 1/3 of the full rate for the first 5 minutes, 2/3 of the full rate for the next 5 minutes, and the full dose rate for the last 20 minutes).

If the investigator believed that an increase to the next higher dose rate would be unsafe, the infusion remained at the current rate for the remainder of the blinded infusion. Since there was no placebo group, the change from baseline likely overestimates the true magnitude of blood pressure effect. Nevertheless, MAP decreased 11 to 20 mmHg from baseline across the four doses ( Table 1 ).

There were 63 pediatric patients in a long-term infusion trial (Study 2). During an open-label phase (12 to 24 hours), sodium nitroprusside was started at 0.3 mcg/kg/min and titrated according to the BP response. Patients were then randomized to placebo or to continuing the same dose of sodium nitroprusside.

The average MAP was greater in the control group than in the sodium nitroprusside group for every time point during the blinded withdrawal phase, demonstrating that sodium nitroprusside is effective for at least 12 hours. In both studies, similar effects on MAP were seen in all age groups. Table 1: Change from Baseline in MAP (mmHg) After 30 Minutes Double-Blind Infusion (Study 1) Dose (mcg/kg/min) Endpoint 0.3 (N=50) 1 (N=49) 2 (N=53) 3 (N=51) Baseline 76 ± 11 77 ± 15 74 ± 12 76 ± 12 30 Min 65 ± 13 60 ± 15 54 ± 12 60 ± 18 Change from Baseline -11 ± 16 (-15, -6.5) -17 ± 13 (-21, -13) -20 ± 16 (-24, -13) -17 ± 19 (-22, -11) Mean ± SD (95% CI)

🧪 Nonclinical Toxicology 62 words ▾

13 NONCLINICAL TOXICOLOGY

13.1Carcinogenesis, Mutagenesis, Impairment of Fertility Animal studies assessing sodium nitroprusside’s carcinogenicity and mutagenicity have not been conducted. Similarly, sodium nitroprusside has not been tested for effects on fertility.

13.2Animal Toxicology and/or Pharmacology The acute intravenous mean lethal doses (LD 50 ) of nitroprusside in rabbits, dogs, mice, and rats are 2.8, 5.0, 8.4, and 11.2 mg/kg, respectively.

📄 Carcinogenesis, Mutagenesis, Impairment of Fertility 29 words ▾

13.1Carcinogenesis, Mutagenesis, Impairment of Fertility Animal studies assessing sodium nitroprusside’s carcinogenicity and mutagenicity have not been conducted. Similarly, sodium nitroprusside has not been tested for effects on fertility.

📄 Package Label / Principal Display Panel 63 words ▾

PACKAGE/LABEL PRINCIPAL DISPLAY PANEL NDC 70436-206-80 Sodium Nitroprusside in 0.9% Sodium Chloride Injection, 20 mg/100 mL (0.5 mg/mL) label 20mgper100mL v1.1

Package/Label Principal Display Panel NDC 70436-207-80 Sodium Nitroprusside in 0.9% Sodium Chloride Injection, 50 mg/100 mL (0.5 mg/mL) label 50mgper100mL v1.1

Package/Label Principal Display Panel NDC 70436-205-80 Sodium Nitroprusside in 0.9% Sodium Chloride Injection, 10 mg/50 mL (0.2 mg/mL) label 10mgper50mL v1.0

Source: FDA Structured Product Labeling, mirrored from DailyMed / openFDA. Prefer the government’s original formatting? View this label on DailyMed ↗

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Why is there no price listed?
The pricing shown on our NDC pages comes from CMS NADAC, a voluntary survey of retail community pharmacy invoices. CMS does not publish a NADAC for every NDC — packages outside the retail survey (institutional and hospital products, bulk packages, discontinued items, and many OTC items) may never receive one. A missing price reflects the survey's scope, not this product's actual cost, and does not mean the product is free or unavailable.
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