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Varubi rolapitant 90 mg Tablet, 2-count — NDC 87628-0101-02 package photo
Label image from the product's FDA listing (DailyMed) — may show a different pack size or an older label revision.

Varubi rolapitant 90 mg Tablet, 2-count — NDC 87628-101-02 (Billing 87628-0101-02)

by Luria Therapeutics LLC · 2 TABLET in 1 BLISTER PACK

This is a package of 2 tablets of Varubi rolapitant 90 mg Tablet from Luria Therapeutics LLC, marketed since Aug 2026 and currently FDA-listed. It is this product's only package size.

NDC 87628-0101-02
🏷️ FDA NDC (as labeled) 87628-101-02 billing pads the product segment with a zero
Rx only Brand On market Non-controlled ⇄ Compare with another NDC
🗂️ FDA directory synced Oct 1, 2026 · this listing last changed Sep 24, 2026 · sources: openFDA · FDA label (DailyMed) · FDA Orange & Purple Book · First Databank · CMS NADAC, ASP, Medicare & Medicaid · RxNorm
📋 All sources & update times →

This page is curated, coded, and maintained by

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) 87628-101-02
Product NDC 87628-101
11-digit billing NDC 87628010102
RxCUI 1665503, 1673373
UNII 57O5S1QSAQ
Application # NDA206500
SPL Set ID 8670c3cf-82d9-466d-be49-de33d8c8742b
Established class (EPC) Substance P/Neurokinin-1 Receptor Antagonist
Mechanism of action Breast Cancer Resistance Protein Inhibitors; Cytochrome P450 2D6 Inhibitors; Neurokinin 1 Antagonists; P-Glycoprotein Inhibitors
DEA schedule Non-controlled
Marketing category NDA
Marketing status On market
FDA listing status Listed (active directory)
Marketing start 2026-08-20
Route ORAL
Dosage form TABLET
Substance ROLAPITANT HYDROCHLORIDE
Quick answers
  • RxCUI (RxNorm): 1665503
Why two NDCs? The FDA registers this code as 87628-101-02 — 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 → 87628-0101-02. 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 Substance P/Neurokinin-1 Receptor Antagonist class.

Pharmacologic class Substance P/Neurokinin-1 Receptor Antagonist
Drug family (ATC) Other antiemetics
How it works Neurokinin 1 Antagonists, Cytochrome P450 2D6 Inhibitors, P-Glycoprotein Inhibitors, Breast Cancer Resistance Protein Inhibitors
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

📗 Our plain-language guide HelloPharmacist
  • It helps prevent delayed nausea and vomiting after cancer chemotherapy in adults. You take it along with other anti-nausea medicines, not by itself.
  • It is a tablet taken by mouth as one dose within 2 hours before chemotherapy starts. You can take it with or without food. It is given before each cycle, at least 2 weeks apart, so...
  • Common ones include low white blood cell counts, hiccups, abdominal pain, decreased appetite, dizziness, indigestion, urinary tract infections and mouth sores. Tell your care team...
  • Yes. Do not take it with thioridazine or pimozide, because it can cause dangerous heart rhythm problems. It can also raise levels of other medicines for at least 28 days, so tell u...
📖 Read our full Rolapitant guide →
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
87628-0101-02 You're viewing this Main listing 2 TABLET in 1 BLISTER PACK 2026-09-08 — Active

Therapeutic equivalents

ProductLabelerPackNADAC/unitTEStatusPrice vs. this
Varubi 90 mg 70720-0101-02 TerSera 2 tablets — — FDA listed —
Varubi 90 mgthis 87628-0101-02 Luria 2 tablets — — FDA listed —
About this product: this is the brand-name version. We did not find an FDA-approved generic match for this exact strength, form and route.
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

🏛️
2015
First FDA approval
Sep 2015
📍
2026
Currently FDA-listed
11 years listed
🛡️
2029
Latest patent/protection listed
not a guaranteed launch date
🔒No FDA-approved generic found

We did not find an FDA-approved generic match for this exact strength, form and route. Patent/protection dates below may affect future generic timing.

🛡️ Latest patent/protection date listed: FDA patent/protection data lists protections through Oct 2029. This may affect when a full generic version becomes widely available, but it is not a guaranteed launch date.
📅 FDA approved Sep 1, 2015 RLD RS ⏳ ~3 yr to latest listed protection

Why the date isn’t exact: Generic timing can change because patents may be challenged, settled, licensed, added, removed, or worked around with a narrower label — and FDA approval does not always mean a pharmacy can get the generic today.

Patents & exclusivity — FDA Orange Book
US 8470842 — method of use (U-1741)
US 8404702 — method of use (U-1741)
US 7981905 — method of use (U-1741)
US 7049320 — drug substance (U-1741)
US 7563801 — drug product
US 8361500 — drug product
US 8178550 — drug substance
2015 2017 2019 2021 2023 2025 2027 2029
Today
LOE
Substance patent Formulation patent Method-of-use patent Exclusivity Pediatric +6mo
🏛️FDA exclusivity
FDA-granted marketing protection. It’s separate from patents and may be shorter than patent protection.
🧪Product / substance patents
Patents covering the active ingredient, product, formulation, or related drug features.
🎯Method-of-use patents
Patents covering specific approved uses. These can sometimes be carved out with a “skinny label,” but not always.
🛈 What do these terms mean?
Patent
Legal protection listed in the Orange Book that may delay generic approval or launch. Issued by the U.S. Patent & Trademark Office.
Substance patent
Covers the active drug molecule itself — the hardest to design around. A generic generally can’t launch until it expires.
Formulation (product) patent
Covers a specific formulation or dosage form. A generic can sometimes work around it with a different formulation.
Method-of-use patent
A patent covering one specific approved use of the drug — not necessarily the whole molecule. A generic can sometimes launch with a “skinny label” that carves out the protected use and keeps the others.
Skinny label
A generic label that omits a still-patented use when the FDA allows it — letting a generic reach the market for the unprotected uses.
Exclusivity
FDA-granted marketing protection, separate from patents — e.g. 5-yr new chemical entity, 7-yr orphan drug, or a +6-month pediatric extension.
Paragraph IV
A generic applicant’s formal challenge to a listed patent. It can potentially lead to earlier generic entry, but often involves litigation or a settlement.
RLD / RS
Reference Listed Drug — the brand product the FDA uses as the reference for generic applications. Reference Standard — the product the FDA expects generics to compare against in bioequivalence testing.
TE / AB rating
FDA therapeutic-equivalence rating. An AB rating generally means the FDA considers a generic therapeutically equivalent to — and substitutable for — the brand.
LOE (loss of exclusivity)
The latest patent or exclusivity currently listed — the loss-of-exclusivity / latest-listed-protection date shown on this page. Paragraph-IV challenges and settlements can move the real date earlier; FDA approval and a manufacturer’s decision to market can move it later.

Built from the FDA Orange Book. The bars above are scaled to each protection’s expiry; the red LOE marker is the last one to lapse.

Listed patents (7)
PatentTypeUse codeExpires
US 8470842 ↗ Method of use U-1741 Jan 18, 2029
US 8404702 ↗ Method of use U-1741 Apr 4, 2027
US 7981905 ↗ Method of use U-1741 Apr 4, 2027
US 7049320 ↗ Drug substance U-1741 Aug 19, 2028
US 7563801 ↗ Drug product — Apr 4, 2027
US 8361500 ↗ Drug product — Oct 9, 2029
US 8178550 ↗ Drug substance — Apr 4, 2027
Common questions
Is there a generic version of this drug?
No FDA-approved generic equivalent is currently listed in the FDA Orange Book for this drug. Based on the patents and exclusivity currently listed, the Orange Book estimate is that full-label generic entry may be delayed until Oct 2029 — an estimate, not a guaranteed launch date.
The FDA approved a generic — why can’t I get it at my pharmacy yet?
FDA approval and pharmacy availability are two different things. The FDA can approve a generic years before it actually reaches pharmacies, because the brand company may still hold patents or have a settlement that delays the launch. A manufacturer also has to choose to make and sell it, and have supply ready. So a drug can be “FDA-approved generic exists” and still be brand-only at the counter today.
Why do different websites show different generic release dates?
Generic availability is not based on one single date. Some sources use the first exclusivity expiration, some use the last product patent, and others use the latest method-of-use patent. Patent challenges, settlements, licenses, and label carve-outs can also change the real-world launch date. This page shows the underlying Orange Book dates so you can see why estimates may differ.
What does “FDA listed” mean?
It means the product appears in the FDA’s official NDC directory. That’s a good sign a product exists and is intended for the U.S. market, but on its own it does not confirm a pharmacy can fill it today. Where we have recent retail pricing data (NADAC) for a product, we label it “Availability likely” instead.
What does a patent or protection date mean here?
It’s the latest date currently listed in the FDA Orange Book for a patent or exclusivity on the brand product. It can affect when a full generic version becomes widely available — but it is not a guaranteed generic launch date. Generics sometimes arrive earlier (through a settlement or patent challenge) or later (a manufacturer still has to make and sell one).
What does “current Orange Book estimate” mean?
It means we are using the latest patent and exclusivity dates currently listed in the FDA Orange Book. It is not a guaranteed launch date.
Can a generic come out before the last patent expires?
Sometimes. A generic company may challenge a patent, settle with the brand manufacturer, receive a license, or obtain approval with a narrower label that avoids a patented use. In other cases, the last listed protection may delay full-label generic competition.
Can a generic come out after the listed dates?
Yes. Even after patents or exclusivity expire, a generic still needs FDA approval and a manufacturer must choose to market it. Supply, litigation, business decisions, or regulatory issues can delay actual availability.
What is the difference between patents and exclusivity?
Patents are legal protections usually issued by the U.S. Patent and Trademark Office. FDA exclusivity is marketing protection granted by the FDA. They are separate, and either one can affect generic timing.
Why are there multiple patent dates?
One drug can have several patents covering different things: the active ingredient, a formulation, a manufacturing process, or a specific approved use. That is why a page may show several expiration dates instead of one simple generic date.
Built from FDA Orange Book patent and exclusivity data. Dates are refreshed from public FDA data when available; the marker is max(latest patent expiry, latest exclusivity expiry). Paragraph-IV settlements and first-filer 180-day exclusivity can shift the real date; a method-of-use patent may allow an earlier skinny-label generic for non-protected indications. Generic launch timing is an estimate, not a guarantee.
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.

What it looks like

Color blue
ShapeOval
ImprintT0101;100
Size15 mm
ScoringNot scored
One label can cover several strengths, so colors may be combined — always confirm a loose pill against the dispensed prescription label or a pharmacist.
Where does this data come from?
Physical description (imprint, shape, color, scoring, coating) from this product’s FDA Structured Product Labeling (SPL), mirrored from DailyMed / openFDA.

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.

💡 Tap an ingredient (hover on desktop) to see what it is and why it’s used.

  • UNII M28OL1HH48
    Croscarmellose sodium is a plant-based substance derived from cellulose. It acts as a disintegrant, helping tablets and capsules break down quickly in the digestive system so the medicine can be absorbed.
  • UNII L06K8R7DQK
    A synthetic blue dye approved by the FDA for use in medications and foods. It serves as a colorant to make pills and liquids visually distinct and easier to identify.
  • UNII EWQ57Q8I5X
    Lactose monohydrate is a natural sugar derived from milk. It serves as a filler and binder in tablets and capsules, helping create the proper size, texture, and consistency of the medicine.
  • UNII 70097M6I30
    Magnesium stearate is a salt made from magnesium and stearic acid, a fatty substance. It's used in tablets and capsules as a lubricant and glidant to help ingredients flow smoothly during manufacturing and prevent sticking.
  • UNII OP1R32D61U
    Microcrystalline cellulose is a purified form of cellulose, a natural fiber from plant sources. It acts as a binder and filler in tablets and capsules, helping hold ingredients together and give the medicine its shape and size.
  • UNII 3WJQ0SDW1A
    Polyethylene glycol is a synthetic liquid or solid polymer used in medicines as a solvent, lubricant, and humectant. It helps dissolve active ingredients, reduces friction during manufacturing, and retains moisture in the final product.
  • UNII 6OZP39ZG8H
    Polysorbate 80 is a synthetic emulsifier derived from sorbitol and oleic acid. It helps mix oil and water-based ingredients together in medications and improves how the product disperses in the body.
  • UNII 532B59J990
    Polyvinyl alcohol is a synthetic polymer made from plant-derived materials. It's used as a binder to hold ingredients together, a film-former in coatings, and a thickener in liquid formulations.
  • UNII FZ989GH94E
    Povidone is a synthetic polymer made from a plastic-like material. It acts as a binder to hold tablet ingredients together and as a disintegrant to help the tablet break apart in your stomach so the medicine can be absorbed.
  • UNII ETJ7Z6XBU4
    Silicon dioxide is a naturally occurring mineral used as a glidant and anti-caking agent. It helps powder ingredients flow smoothly and prevents clumping during manufacturing and storage.
  • UNII O8232NY3SJ
    A plant-based carbohydrate derived from corn kernels. It acts as a filler to add bulk, a binder to hold ingredients together, and a disintegrant to help the tablet break apart in your stomach for absorption.
  • UNII 7SEV7J4R1U
    A powder made from a naturally occurring mineral. In medicines, talc works as a glidant and anti-caking agent, helping tablets and capsules flow smoothly during manufacturing and preventing clumping.
  • UNII 15FIX9V2JP
    Titanium dioxide is a bright white mineral powder commonly used as a colorant and opacifying agent. It makes pills and tablets white or lighter in color and helps make coatings non-transparent.

13 inactive ingredients listed in the exact product block matched to this NDC.

Where does this data come from?
Data sourced from official FDA Structured Product Labeling (SPL) via DailyMed — ingredient classCode="IACT" elements from the exact product block matched by this NDC. Label-section narrative from DailyMed / the openFDA label index is shown separately when available.

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

LabelerLuria Therapeutics LLC
Application holderTERSERA THERAPEUTICS LLC
FDA applicationNDA206500 (NDA)
Labeler code87628
First marketedAug 2026
Product typeHuman Prescription Drug
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.
🎯 Indications and Usage ⏱️ Dosage and Administration 💊 Dosage Forms and Strengths ⛔ Contraindications ⚠️ Warnings and Cautions 🤒 Adverse Reactions 🔄 Drug Interactions 👥 Use in Specific Populations 🤰 Pregnancy 🧒 Pediatric Use 🧓 Geriatric 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 📄 Patient Package Insert 📄 Package Label / Principal Display Panel
🎯 Indications and Usage 89 words ▾

1 INDICATIONS AND USAGE VARUBI ® is indicated in combination with other antiemetic agents in adults for the prevention of delayed nausea and vomiting associated with initial and repeat courses of emetogenic cancer chemotherapy, including, but not limited to, highly emetogenic chemotherapy. VARUBI is a substance P/neurokinin 1 (NK1) receptor antagonist indicated in combination with other antiemetic agents in adults for the prevention of delayed nausea and vomiting associated with initial and repeat courses of emetogenic cancer chemotherapy, including, but not limited to, highly emetogenic chemotherapy.

( 1 )

⏱️ Dosage and Administration ~2 min read ▾

2 DOSAGE AND ADMINISTRATION The recommended dosage of VARUBI in adults in combination with a 5-HT 3 receptor antagonist and dexamethasone for the prevention of nausea and vomiting with emetogenic cancer chemotherapy is shown in Table 1 . There is no drug interaction between rolapitant and dexamethasone, so no dosage adjustment for dexamethasone is required. Administer a dexamethasone dose of 20 mg on Day 1 [see Clinical Pharmacology (12.3) ] .

Administer VARUBI prior to the initiation of each chemotherapy cycle, but at no less than 2 week intervals. Administer VARUBI without regards to meals. Table 1: Recommended Dosing Regimen of VARUBI Day 1 Day 2 Day 3 Day 4 Prevention of Nausea and Vomiting Associated with Cisplatin-Based Highly Emetogenic Cancer Chemotherapy VARUBI 180 mg as a single dose orally within 2 hours prior to initiation of chemotherapy None Dexamethasone 20 mg; 30 min prior to initiation of chemotherapy 8 mg twice daily 8 mg twice daily 8 mg twice daily 5-HT 3 receptor antagonist See the prescribing information for the co-administered 5-HT 3 receptor antagonist for appropriate dosing information.

None Prevention of Nausea and Vomiting Associated with Moderately Emetogenic Cancer Chemotherapy and Combinations of Anthracycline and Cyclophosphamide VARUBI 180 mg as a single dose orally within 2 hours prior to initiation of chemotherapy None Dexamethasone 20 mg; 30 min prior to initiation of chemotherapy None 5-HT 3 receptor antagonist See the prescribing information for the co-administered 5-HT 3 receptor antagonist for appropriate dosing information. See the prescribing information for the co-administered 5-HT 3 receptor antagonist for appropriate dosing information.

Administer in combination with dexamethasone and a 5-HT 3 receptor antagonist; see full prescribing information for dosing information. ( 2 ) No dosage adjustment for dexamethasone is required. ( 2 ) The recommended dosage of VARUBI is 180 mg as a single dose orally within 2 hours prior to the initiation of chemotherapy on Day 1.

( 2 ) Administer VARUBI prior to the initiation of each chemotherapy cycle, but at no less than 2 week intervals. ( 2 ) Administer VARUBI without regards to meals. ( 2 )

💊 Dosage Forms and Strengths 33 words ▾

3 DOSAGE FORMS AND STRENGTHS Tablets: 90 mg rolapitant; film-coated, blue capsule shaped, debossed with T0101 on one side and 100 on the other side. Tablets: 90 mg of rolapitant ( 3 )

⛔ Contraindications 128 words ▾

4 CONTRAINDICATIONS VARUBI is contraindicated in patients taking CYP2D6 substrates with a narrow therapeutic index, such as thioridazine and pimozide. VARUBI can significantly increase the plasma concentrations of thioridazine and pimozide, which may result in QT prolongation and Torsades de Pointes [see Warnings and Precautions (5.1) ] . VARUBI is contraindicated in pediatric patients less than 2 years of age because of irreversible impairment of sexual development and fertility observed in juvenile rats at clinically relevant dosages [see Use in Specific Populations (8.4) ] .

CYP2D6 substrates with a narrow therapeutic index (e.g., thioridazine and pimozide) ( 4 , 5.1 , 7 ) Pediatric patients less than 2 years of age because of irreversible impairment of sexual development and fertility in juvenile rats ( 4 , 8.4 )

⚠️ Warnings and Cautions ~1 min read ▾

5 WARNINGS AND PRECAUTIONS CYP2D6 Substrates : Rolapitant is a moderate inhibitor of CYP2D6 and significantly increases the plasma concentrations of CYP2D6 substrates for at least 28 days following single dose administration of VARUBI. Before starting VARUBI, consider if patients require: thioridazine or pimozide; if so, use an alternative antiemetic to VARUBI or an alternative to thioridazine or pimozide that is not metabolized by CYP2D6. other CYP2D6 substrates; if so, consult the prescribing information for the CYP2D6 substrate for additional information about interactions with CYP2D6 inhibitors.

( 4 , 5.1 , 7 )

5.1Interaction with CYP2D6 Substrates Rolapitant is a moderate inhibitor of CYP2D6. Exposure to dextromethorphan, a CYP2D6 substrate, following a single dose of rolapitant increased about 3-fold on Days 8 and Day 22. The inhibition of CYP2D6 persisted on Day 28 with a 2.3-fold increase in dextromethorphan (CYP2D6 substrate) concentrations, the last time point measured.

The inhibitory effect of rolapitant on CYP2D6 is expected to persist beyond 28 days for an unknown duration following administration of VARUBI [see Drug Interactions (7) , Clinical Pharmacology (12.3) ] . Narrow Therapeutic Index Drugs (Thioridazine and Pimozide) VARUBI is contraindicated in patients taking CYP2D6 substrates with a narrow therapeutic index such as thioridazine and pimozide. Increased plasma concentrations of thioridazine and pimozide are associated with serious and/or life-threatening events of QT prolongation and Torsades de Pointes [see Contraindications (4) ] .

Before starting treatment with VARUBI, consider whether patients require treatment with thioridazine or pimozide. If patients require these drugs, use an alternative antiemetic to VARUBI or an alternative to thioridazine or pimozide that is not metabolized by CYP2D6. Other Drugs VARUBI can also increase plasma concentrations of other CYP2D6 substrates for at least 28 days following administration of VARUBI and may result in adverse reactions.

Before starting treatment with VARUBI, consult the prescribing information for CYP2D6 substrates to obtain additional information about interactions with CYP2D6 inhibitors.

🤒 Adverse Reactions ~2 min read ▾

6 ADVERSE REACTIONS The following adverse reactions are discussed in greater detail in other sections of the labeling: Interaction with CYP2D6 Substrates [see Contraindications (4) , Warnings and Precautions (5.1) ] Most common adverse reactions (≥3%) are: Cisplatin Based Highly Emetogenic Chemotherapy: neutropenia, hiccups and abdominal pain. ( 6.1 ) Moderately Emetogenic Chemotherapy and Combinations of Anthracycline and Cyclophosphamide: decreased appetite, neutropenia, dizziness, dyspepsia, urinary tract infection, stomatitis and anemia.

( 6.1 ) To report SUSPECTED ADVERSE REACTIONS, contact Luria Therapeutics LLC at 1-844-334-4035 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

6.1Clinical Trials Experience Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice. In 4 controlled clinical trials in patients receiving emetogenic cancer chemotherapy, VARUBI was given in combination with a 5-HT 3 receptor antagonist and dexamethasone. On Day 1 of Cycle 1 of chemotherapy, 1567 patients were treated with VARUBI and 1198 of these patients continued into the optional multiple cycle extension for up to 6 cycles of chemotherapy.

The median number of cycles administered 180 mg of VARUBI was four. VARUBI 180 mg was administered to 1294 patients. In Cycle 1 adverse reactions were reported in approximately 7% of patients treated with VARUBI compared with approximately 6% of patients treated with control therapy.

The most common adverse reactions reported with an incidence of ≥3% and greater than control are listed in Table 2 and Table 3 . Table 2: Most Common Adverse Reactions in Patients Receiving Cisplatin-Based Highly Emetogenic Chemotherapy (Cycle 1)* * all reactions occurring at ≥3% in the VARUBI group and for which the rate for VARUBI exceeds the rate for control VARUBI Regimen (VARUBI, Dexamethasone, and 5-HT 3 Receptor Antagonist) N = 624 Control (Placebo, Dexamethasone, and 5-HT 3 Receptor Antagonist) N = 627 Neutropenia 9% 8% Hiccups 5% 4% Abdominal Pain 3% 2% Table 3: Most Common Adverse Reactions in Patients Receiving Moderately Emetogenic Chemotherapy and Combinations of Anthracycline and Cyclophosphamide (Cycle 1)* *all reactions occurring at ≥3% in the VARUBI group and for which the rate for VARUBI exceeds the rate for control.

VARUBI Regimen (VARUBI, Dexamethasone, and 5-HT 3 Receptor Antagonist) N = 670 Control (Placebo, Dexamethasone, and 5-HT 3 Receptor Antagonist) N = 674 Decreased appetite 9% 7% Neutropenia 7% 6% Dizziness 6% 4% Dyspepsia 4% 2% Urinary tract infection 4% 3% Stomatitis 4% 2% Anemia 3% 2% Adverse reactions in the multiple-cycle extensions of highly and moderately emetogenic chemotherapy studies for up to 6 cycles of chemotherapy were generally similar to that observed in Cycle 1.

🔄 Drug Interactions ~3 min read ▾

7 DRUG INTERACTIONS Rolapitant is a moderate CYP2D6 inhibitor. The inhibition of CYP2D6 persisted on Day 28 with a 2.3-fold increase in dextromethorphan concentrations, the last time point measured. The inhibitory effect of rolapitant on CYP2D6 is expected to persist beyond 28 days for an unknown duration following administration of VARUBI [see Clinical Pharmacology (12.3) ] .

Oral rolapitant is an inhibitor of Breast-Cancer-Resistance Protein (BCRP) and p-glycoprotein (P-gp). Rolapitant, given as a single oral dose, is not an inhibitor or inducer of CYP3A4 [see Clinical Pharmacology (12.3) ] . Therefore, no dosage adjustment for dexamethasone (CYP3A4 substrate) is needed when co-administered with VARUBI [see Dosage and Administration (2) ] .

Table 4 and Table 5 include drugs with clinically important drug interactions when administered concomitantly with VARUBI and instructions for preventing or managing them. Table 4: Clinically Relevant Interactions Affecting Drugs Co-Administered with VARUBI CYP2D6 Substrates Narrow Therapeutic Index Drugs (Thioridazine and Pimozide) Clinical Impact: Increased plasma concentrations of thioridazine and pimozide are associated with serious and/or life-threatening events of QT prolongation and Torsades de Pointes. Intervention: VARUBI is contraindicated in patients taking CYP2D6 substrates with a narrow therapeutic index such as thioridazine and pimozide.

If patients require these drugs, use an alternative antiemetic to VARUBI or an alternative to thioridazine or pimozide that is not metabolized by CYP2D6 [see Contraindications (4) , Warnings and Precautions (5.1) ]. Other CYP2D6 Substrates Clinical Impact: VARUBI can increase plasma concentrations of other CYP2D6 substrates for at least 28 days following administration of VARUBI and may result in adverse reactions. Before starting treatment with VARUBI consult the prescribing information of CYP2D6 substrates to obtain further information about interactions with CYP2D6 inhibitors [see Clinical Pharmacology (12.3) ].

Intervention: Before starting treatment with VARUBI consult the prescribing information of CYP2D6 substrates to obtain further information about interactions with CYP2D6 inhibitors [see Warnings and Precautions (5.1) ]. BCRP Substrates with a Narrow Therapeutic Index (e.g., methotrexate, topotecan, or irinotecan) Clinical Impact: Increased plasma concentrations of BCRP substrates (e.g., methotrexate, topotecan, or irinotecan) may result in potential adverse reactions [see Clinical Pharmacology (12.3) ]. Intervention: Monitor for adverse reactions related to the concomitant drug if use of VARUBI cannot be avoided.

Use the lowest effective dose of rosuvastatin (see prescribing information for additional information on recommended dosing). P-gp Substrates with a Narrow Therapeutic Index (e.g. digoxin) Clinical Impact: Increased plasma concentrations of P-gp substrates (e.g., digoxin) may result in potential adverse reactions [see Clinical Pharmacology (12.3) ]. Intervention: Monitor digoxin concentrations with concomitant use of VARUBI and adjust the dosage as needed to maintain therapeutic concentrations.

Monitor for adverse reactions if concomitant use of VARUBI with other P-gp substrates with a narrow therapeutic index cannot be avoided. Warfarin Clinical Impact: Although co-administration of intravenous rolapitant (VARBI is not approved for intravenous use), which has a higher C max than oral VARUBI, with warfarin did not substantially increase the systemic exposure to S-warfarin, the active enantiomer, the effects on INR and prothrombin time were not studied [see Clinical Pharmacology (12.3) ] . Intervention: Monitor INR and prothrombin time and adjust the dosage of warfarin, as needed with concomitant use of VARUBI, to maintain the target INR range.

Table 5: Clinically Relevant Interactions Affecting Rolapitant When Co-Administered with Other Drugs Strong CYP3A4 Inducers (e.g. rifampin) Clinical Impact: Co-administration of VAR… [Excerpted — this section continues on DailyMed.]

👥 Use in Specific Populations ~3 min read ▾

8 USE IN SPECIFIC POPULATIONS

8.1Pregnancy Risk Summary The limited data with VARUBI use in pregnant women are insufficient to inform a drug associated risk of adverse developmental outcomes. In animal reproduction studies, there were no adverse developmental effects observed with oral administration of rolapitant in rats and rabbits during the period of organogenesis at doses up to 1.2 times and 2.9-times, respectively, the maximum recommended human dose (MRHD) (see Data ) . 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 to 4% and 15 to 20%, respectively. Data Animal Data The potential embryo-fetal toxicity of rolapitant was assessed in pregnant rats administered oral doses up to 22.5 mg/kg per day throughout the period of organogenesis.

Rats administered doses of 13.5 or 22.5 mg/kg per day rolapitant exhibited evidence of maternal toxicity including decreased body weight gain and/or body weight loss and a concomitant decrease in food consumption during the first week of dosing. No adverse embryo-fetal developmental effects were observed at doses up to 22.5 mg/kg per day rolapitant (approximately 1.2 times the recommended human dose on a body surface area basis). In rabbits administered rolapitant throughout the period of organogenesis, oral doses up to 27 mg/kg per day (approximately 2.9 times the recommended human dose on a body surface area basis) were without effects on the developing fetus.

The pre- and postnatal developmental effects of rolapitant were assessed in rats administered oral doses of 2.25, 9 or 22.5 mg/kg per day during the periods of organogenesis and lactation. Maternal toxicity was evident based on mortality/moribund condition, decreased body weight and food consumption, total litter loss, prolonged parturition, decreased length of gestation, and increased number of unaccounted for implantation sites at a dose of 22.5 mg/kg per day (approximately 1.2 times the recommended human dose on a body surface area basis).

Effects on offspring at this dose included decreased postnatal survival, and decreased body weights and body weight gain, and may be related to the maternal toxicity observed. At a maternal dose of 9 mg/kg per day rolapitant (approximately 0.5 times the recommended human dose on a body surface area basis), there was a decrease in memory in female pups in a maze test and a decrease in pup body weight.

8.2Lactation Risk Summary There are no data on the presence of rolapitant in human milk, the effects of rolapitant in the breastfed infant, or the effects of rolapitant on milk production. Rolapitant administered orally to lactating female rats was present in milk (see Data ) . The developmental and health benefits of breastfeeding should be considered along with the mother's clinical need for VARUBI and any potential adverse effects on the breastfed infant from VARUBI or from the underlying maternal condition or the use of concomitant chemotherapy.

Data Radioactivity from labeled [ 14 C] rolapitant was transferred into milk of lactating rats following a single oral dose of 22.5 mg/kg, and the maximum radioactivity in milk was observed at 12 hours post-dose. The mean milk/plasma radioactivity concentration ratios in dams at 1 to 48 hours post-dose ranged from 1.24 to 3.25. Based on average daily consumption of milk (2 mL/day) and the maximum milk radioactivity determined, pup exposure is expected to be 0.3% of the orally administered dose.

8.3Females and Males of Reproductive Potential Infertility Females In animal fertility studies, rolapitant impaired the fertility in females in a reversible fashion [see Nonclinical Toxicology (13.1) ] .

8.4Pediatric Use The safety and effectiveness of VARUBI have not bee… [Excerpted — this section continues on DailyMed.]

🤰 Pregnancy ~2 min read ▾

8.1Pregnancy Risk Summary The limited data with VARUBI use in pregnant women are insufficient to inform a drug associated risk of adverse developmental outcomes. In animal reproduction studies, there were no adverse developmental effects observed with oral administration of rolapitant in rats and rabbits during the period of organogenesis at doses up to 1.2 times and 2.9-times, respectively, the maximum recommended human dose (MRHD) (see Data ) . 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 to 4% and 15 to 20%, respectively. Data Animal Data The potential embryo-fetal toxicity of rolapitant was assessed in pregnant rats administered oral doses up to 22.5 mg/kg per day throughout the period of organogenesis.

Rats administered doses of 13.5 or 22.5 mg/kg per day rolapitant exhibited evidence of maternal toxicity including decreased body weight gain and/or body weight loss and a concomitant decrease in food consumption during the first week of dosing. No adverse embryo-fetal developmental effects were observed at doses up to 22.5 mg/kg per day rolapitant (approximately 1.2 times the recommended human dose on a body surface area basis). In rabbits administered rolapitant throughout the period of organogenesis, oral doses up to 27 mg/kg per day (approximately 2.9 times the recommended human dose on a body surface area basis) were without effects on the developing fetus.

The pre- and postnatal developmental effects of rolapitant were assessed in rats administered oral doses of 2.25, 9 or 22.5 mg/kg per day during the periods of organogenesis and lactation. Maternal toxicity was evident based on mortality/moribund condition, decreased body weight and food consumption, total litter loss, prolonged parturition, decreased length of gestation, and increased number of unaccounted for implantation sites at a dose of 22.5 mg/kg per day (approximately 1.2 times the recommended human dose on a body surface area basis).

Effects on offspring at this dose included decreased postnatal survival, and decreased body weights and body weight gain, and may be related to the maternal toxicity observed. At a maternal dose of 9 mg/kg per day rolapitant (approximately 0.5 times the recommended human dose on a body surface area basis), there was a decrease in memory in female pups in a maze test and a decrease in pup body weight.

🧒 Pediatric Use ~1 min read ▾

8.4Pediatric Use The safety and effectiveness of VARUBI have not been established in pediatric patients. VARUBI is contraindicated in pediatric patients less than 2 years of age [see Contraindications(4) ]. Rolapitant administration in juvenile rats (human age equivalent of birth to 2 years) resulted in abnormal ovarian and uterine development, early sexual development in females, delayed sexual development in males, and impaired fertility.

Juvenile Animal Toxicity Data A toxicity study in juvenile rats at rolapitant doses approximately 1.2 and 2.5 times the approved adult body surface area (BSA)-based dose from postnatal day (PND) 7 through PND 70 (approximate human age equivalent of birth to 16 years) identified reproductive toxicity. A subsequent toxicity study in juvenile rats was conducted to identify the critical window of exposure for reproductive toxicity. A rolapitant dose of 50 mg/kg/day (approximately 2.7 times the approved adult BSA-based dose) was administered daily from PNDs 7 through 70, 7 to 21, 21 to 42 and 42 to 70 (approximate human age equivalent of birth to 16 years, birth to 2 years, 2 years to 12 years, and 12 years to 16 years, respectively).

Female juvenile rats treated with rolapitant beginning on PND 7 developed adverse effects including partial or irreversible lower uterine weights that correlated with decreased endometrial glands of the uterus, decreases in the numbers of corpora lutea, implantation sites and live embryos and increases in pre- and post-implantation loss, and early resorptions. These adverse effects were observed in female juvenile rats administered rolapitant prior to PND 21 (approximate human age equivalent of 2 years). Additionally, juvenile rats treated with rolapitant beginning on either PND 7 or PND 21 developed slight changes in the onset of sexual maturation (including earlier attainment of vaginal opening in females and delay in preputial separation in males).

🧓 Geriatric Use 49 words ▾

8.5Geriatric Use Of the 1294 subjects treated with VARUBI, 25% were 65 years and over, while 5% were 75 and over. No overall differences in safety or efficacy were reported between the elderly subjects and younger subjects, but greater sensitivity of some older individuals cannot be ruled out.

🆘 Overdosage 32 words ▾

10 OVERDOSAGE There are no data on overdose with VARUBI. There is no antidote for VARUBI overdose. Discontinue VARUBI in the event of overdose, and institute general supportive measures and close observation.

🧬 Clinical Pharmacology ~3 min read ▾

12 CLINICAL PHARMACOLOGY

12.1Mechanism of Action Rolapitant is a selective and competitive antagonist of human substance P/NK1 receptors. Rolapitant does not have significant affinity for the NK2 or NK3 receptors or for a battery of other receptors, transporters, enzymes and ion channels. Rolapitant is also active in animal models of chemotherapy-induced emesis.

12.2Pharmacodynamics NK1 Receptor Occupancy A human Positron Emission Tomography (PET) study with rolapitant demonstrated that rolapitant crosses the blood brain barrier and occupies brain NK1 receptors. A dose-dependent increase in mean NK1 receptor occupancy was observed in the oral dose range from 4.5 mg to 180 mg of rolapitant. At the 180 mg oral dose of rolapitant, the mean NK1 receptor occupancy was 73% in the striatum at 120 hours after a single dose administration in healthy subjects.

The relationship between NK1 receptor occupancy and the clinical efficacy of rolapitant has not been established. Cardiac Electrophysiology At an oral dose of 720 mg (4 times the recommended oral dose), VARUBI does not prolong the QT interval to any clinically relevant extent.

12.3Pharmacokinetics Absorption Following a single oral dose administration of 180 mg VARUBI under fasting conditions to healthy subjects, rolapitant was measurable in plasma within 30 minutes and the peak plasma concentration (C max ) for rolapitant which was reached in about 4 hours and mean C max was 968 ng/mL (%CV:28%). Following multiple oral doses of 9 to 45 mg once daily of rolapitant (5% to 25% of the recommended dose) for 10 days, accumulation of rolapitant (ratio of AUC 0-24hr ) ranged from 5.0 to 5.3 fold.

The systemic exposures (C max and AUC) to rolapitant increased in a dose-proportional manner when single oral doses of rolapitant increased from 4.5 mg to 180 mg. With 4 times the recommended clinical oral dose of 180 mg, the C max and AUC of rolapitant increased 3.1 fold and 3.7 fold, respectively. Concomitant administration of a high-fat meal did not significantly affect the pharmacokinetics of rolapitant after administration of 180 mg VARUBI [see Dosage and Administration (2) ] .

Distribution Rolapitant was highly protein bound to human plasma (99.8%). The apparent volume of distribution (Vd/F) following a single oral dose of 180 mg rolapitant was 460 L in healthy subjects. The large Vd indicated an extensive tissue distribution of rolapitant.

In a population pharmacokinetic analysis of oral rolapitant, the Vd/F was 387 L in cancer patients. Elimination Following single oral doses (4.5 to 180 mg) of rolapitant, the mean terminal half-life (t 1/2 ) of rolapitant ranged from 169 to 183 hours (approximately 7 days), and was independent of dose. In a population pharmacokinetic analysis, the apparent total clearance (CL/F) of oral rolapitant was

0.96L/hour in cancer patients. Metabolism Rolapitant is metabolized primarily by CYP3A4 to form a major active metabolite, M19 (C4-pyrrolidine-hydroxylated rolapitant). In a mass balance study, the metabolite M19 was determined to be the major circulating metabolite.

The rate of formation of M19 was relatively slow, resulting in the delayed median T max of 120 hours (range: 24 to 168 hours) with C max of 183 ng/mL. The mean half-life of M19 was 158 hours. The exposure ratio of M19 to rolapitant was approximately 50% in plasma.

Excretion Rolapitant is eliminated primarily through the hepato/biliary route. Following administration of a single oral 180-mg dose of [ 14 C]-rolapitant, on average 14.2% (range 9% to 20%) and 73% (range 52% to 89%) of the dose was recovered in the urine and feces, respectively over 6 weeks. In pooled samples collected over 2 weeks, 8.3% of the dose was recovered in the urine primarily as metabolites and 37.8% of the dose was recovered in the feces primarily as unchanged rolapitant.

Unchanged rolapitant or M19 was not found in pooled urine sample. Specific Populations Age, Male and Female Patients and Racial or Ethnic Groups Po… [Excerpted — this section continues on DailyMed.]

🧬 Mechanism of Action 50 words ▾

12.1Mechanism of Action Rolapitant is a selective and competitive antagonist of human substance P/NK1 receptors. Rolapitant does not have significant affinity for the NK2 or NK3 receptors or for a battery of other receptors, transporters, enzymes and ion channels. Rolapitant is also active in animal models of chemotherapy-induced emesis.

📦 How Supplied / Storage and Handling 85 words ▾

16 HOW SUPPLIED/STORAGE AND HANDLING VARUBI is available as film-coated, capsule shaped, blue tablets, debossed with T0101 on one side and 100 on the other side. Each tablet contains 90 mg rolapitant. VARUBI is packaged in an Aclar blister shell with aluminum foil backing and supplied as follows: NDC 87628-101-02 A single dose child-resistant wallet (2 tablets as one set of twinned blisters) Store at 20ºC to 25ºC (68ºF to 77ºF); excursions permitted to 15°C to 30°C (59°F to 86°F) [see USP Controlled Room Temperature].

📋 Description 161 words ▾

11 DESCRIPTION VARUBI contains rolapitant, a substance P/neurokinin 1 (NK1) receptor antagonist. Rolapitant hydrochloride is chemically described as (5S,8S)-8- { [(1R)-1-[3,5-bis(trifluoromethyl)phenyl]ethoxy]methyl]}-8-phenyl-1,7-diazaspiro[4.5]decan-2-one hydrochloride. Its empirical formula is C 25 H 26 F 6 N 2 O 2 .

HCl.H 2 O, and its structural formula is: rolapitant hydrochloride Rolapitant hydrochloride is a white to off-white powder, with a molecular weight of 554.95. Solubility of rolapitant hydrochloride in aqueous solution is pH-dependent and is more soluble at lower pH. Rolapitant has good solubility in common pharmaceutical solvents such as ethanol, propylene glycol and 40% hydroxypropyl beta-cyclodextrin.

Each tablet contains 90 mg rolapitant (equivalent to 100 mg rolapitant hydrochloride) and the following inactive ingredients: colloidal silicon dioxide, croscarmellose sodium, lactose monohydrate, magnesium stearate, microcrystalline cellulose, povidone, and pregelatinized starch. The tablets are coated in non-functional blue and clear coats. The tablet coating comprises the following inactive ingredients: FD&C Blue No.

2-Indigo Carmine Lake, polyethylene glycol, polysorbate 80, polyvinyl alcohol, talc, and titanium dioxide. Figure

💬 Information for Patients 93 words ▾

17 PATIENT COUNSELING INFORMATION Advise the patient to read the FDA-approved patient labeling (Patient Information). Drug Interactions Advise patients to tell their healthcare provider when they start or stop taking any concomitant medications. VARUBI is a moderate CYP2D6 inhibitor and can increase plasma concentrations of CYP2D6 substrates [see Contraindications (4) , Warnings and Precautions (5.1) , Drug Interactions (7) ] .

Infertility Advise females of reproductive potential that VARUBI may impair fertility [see Use in Specific Populations (8.3) , Nonclinical Toxicology (13.1) ] . Distributed by: Luria Therapeutics LLC, Pleasant Prairie, WI 53158

🧬 Pharmacokinetics ~3 min read ▾

12.3Pharmacokinetics Absorption Following a single oral dose administration of 180 mg VARUBI under fasting conditions to healthy subjects, rolapitant was measurable in plasma within 30 minutes and the peak plasma concentration (C max ) for rolapitant which was reached in about 4 hours and mean C max was 968 ng/mL (%CV:28%). Following multiple oral doses of 9 to 45 mg once daily of rolapitant (5% to 25% of the recommended dose) for 10 days, accumulation of rolapitant (ratio of AUC 0-24hr ) ranged from 5.0 to 5.3 fold.

The systemic exposures (C max and AUC) to rolapitant increased in a dose-proportional manner when single oral doses of rolapitant increased from 4.5 mg to 180 mg. With 4 times the recommended clinical oral dose of 180 mg, the C max and AUC of rolapitant increased 3.1 fold and 3.7 fold, respectively. Concomitant administration of a high-fat meal did not significantly affect the pharmacokinetics of rolapitant after administration of 180 mg VARUBI [see Dosage and Administration (2) ] .

Distribution Rolapitant was highly protein bound to human plasma (99.8%). The apparent volume of distribution (Vd/F) following a single oral dose of 180 mg rolapitant was 460 L in healthy subjects. The large Vd indicated an extensive tissue distribution of rolapitant.

In a population pharmacokinetic analysis of oral rolapitant, the Vd/F was 387 L in cancer patients. Elimination Following single oral doses (4.5 to 180 mg) of rolapitant, the mean terminal half-life (t 1/2 ) of rolapitant ranged from 169 to 183 hours (approximately 7 days), and was independent of dose. In a population pharmacokinetic analysis, the apparent total clearance (CL/F) of oral rolapitant was

0.96L/hour in cancer patients. Metabolism Rolapitant is metabolized primarily by CYP3A4 to form a major active metabolite, M19 (C4-pyrrolidine-hydroxylated rolapitant). In a mass balance study, the metabolite M19 was determined to be the major circulating metabolite.

The rate of formation of M19 was relatively slow, resulting in the delayed median T max of 120 hours (range: 24 to 168 hours) with C max of 183 ng/mL. The mean half-life of M19 was 158 hours. The exposure ratio of M19 to rolapitant was approximately 50% in plasma.

Excretion Rolapitant is eliminated primarily through the hepato/biliary route. Following administration of a single oral 180-mg dose of [ 14 C]-rolapitant, on average 14.2% (range 9% to 20%) and 73% (range 52% to 89%) of the dose was recovered in the urine and feces, respectively over 6 weeks. In pooled samples collected over 2 weeks, 8.3% of the dose was recovered in the urine primarily as metabolites and 37.8% of the dose was recovered in the feces primarily as unchanged rolapitant.

Unchanged rolapitant or M19 was not found in pooled urine sample. Specific Populations Age, Male and Female Patients and Racial or Ethnic Groups Population pharmacokinetic analyses indicated that age, sex and race had no significant impact on the pharmacokinetics of rolapitant. Patients with Hepatic Impairment Following administration of a single oral dose of 180 mg rolapitant to patients with mild hepatic impairment (Child-Pugh Class A), the pharmacokinetics of rolapitant were comparable with those of healthy subjects.

In patients with moderate hepatic impairment (Child-Pugh Class B), the mean C max was 25% lower while mean AUC of rolapitant was similar compared to those of healthy subjects. The median T max for M19 was delayed to 204 hours in patients with mild or moderate hepatic impairment compared to 168 hours in healthy subjects. The pharmacokinetics of rolapitant were not studied in patients with severe hepatic impairment (Child-Pugh Class C) [see Use in Specific Populations (8.6) ] .

Patients with Renal Impairment In population pharmacokinetic analyses, rolapitant pharmacokinetics in cancer patients with mild (CLcr: 60 to 90 mL/min) or moderate (CLcr: 30 to 60 mL/min) renal impairment was comparable to cancer patients with normal kidney function. Information is… [Excerpted — this section continues on DailyMed.]

🧬 Pharmacodynamics 122 words ▾

12.2Pharmacodynamics NK1 Receptor Occupancy A human Positron Emission Tomography (PET) study with rolapitant demonstrated that rolapitant crosses the blood brain barrier and occupies brain NK1 receptors. A dose-dependent increase in mean NK1 receptor occupancy was observed in the oral dose range from 4.5 mg to 180 mg of rolapitant. At the 180 mg oral dose of rolapitant, the mean NK1 receptor occupancy was 73% in the striatum at 120 hours after a single dose administration in healthy subjects.

The relationship between NK1 receptor occupancy and the clinical efficacy of rolapitant has not been established. Cardiac Electrophysiology At an oral dose of 720 mg (4 times the recommended oral dose), VARUBI does not prolong the QT interval to any clinically relevant extent.

🔬 Clinical Studies ~3 min read ▾

14 CLINICAL STUDIES Cisplatin-Based Highly Emetogenic Chemotherapy (HEC) In two multicenter, randomized, double-blind, parallel group, controlled clinical studies (Study 1 and Study 2), the VARUBI regimen (VARUBI, granisetron and dexamethasone) was compared with control therapy (placebo, granisetron and dexamethasone) in patients receiving a chemotherapy regimen that included cisplatin >60 mg/m 2 . See Table 7 for the treatment regimens. Table 7: Treatment Regimens in Studies 1 and 2 a VARUBI was administered 1 to 2 hours prior to chemotherapy treatment on Day 1. b Dexamethasone was administered 30 minutes prior to chemotherapy on Day 1.

There is no drug interaction between VARUBI and dexamethasone, so no dosage adjustment for dexamethasone is required [see Clinical Pharmacology (12.3) ] . c The dose of granisetron was administered 30 minutes prior to chemotherapy on Day 1. d VARUBI placebo was used to maintain blinding. Day 1 Day 2 to 4 VARUBI Regimen Oral VARUBI a 180 mg None Oral Dexamethasone 20 mg b 8 mg twice daily Intravenous Granisetron 10 mcg/kg c None Control Regimen d Oral Dexamethasone 20 mg b 8 mg twice daily Intravenous Granisetron 10 mcg/kg c None Study 1 A total of 532 patients were randomized to either the VARUBI regimen (N=266) or control therapy (N=266).

A total of 526 patients were included in the evaluation of efficacy. Of those randomized 42% were women, 58% men, 67% White, 23% Asian, 1% Black, and 9% multi-racial/other/unknown. The proportion of patients from North America was 16%.

Patients in this clinical study ranged from 20 to 90 years of age, with a mean age of 57 years. In Study 1, 26% of patients were 65 years or older, with 3% of patients being 75 years or older. The mean cisplatin dose was 77 mg/m 2 .

During this study, 82% of the patients received a concomitant chemotherapeutic agent in addition to protocol-mandated cisplatin. The most common concomitant chemotherapeutic agents administered during Cycle 1 were: gemcitabine (17%), paclitaxel (12%), fluorouracil (11%), etoposide (10%), vinorelbine (9%), docetaxel (9%), pemetrexed (7%), doxorubicin (6%) and cyclophosphamide (5%). Study 2 A total of 555 patients were randomized to either the VARUBI regimen (N=278) or control therapy (N=277).

A total of 544 patients were included in the evaluation of efficacy. Of those randomized 32% were women, 68% men, 81% White, 14% Asian, 1% Black, and 5% multi-racial/other/unknown. The proportion of patients from North America was 7%.

Patients in this clinical study ranged from 18 to 83 years of age, with a mean age of 58 years. In this study, 27% of patients were 65 years or older, with 3% of patients being 75 years or older. The mean cisplatin dose was 76 mg/m 2 .

During this study, 85% of the patients received a concomitant chemotherapeutic agent in addition to protocol-mandated cisplatin. The most common concomitant chemotherapeutic agents administered during Cycle 1 were: vinorelbine (16%), gemcitabine (15%), fluorouracil (12%), etoposide (11%), pemetrexed (9%), docetaxel (7%), paclitaxel (7%), epirubicin (5%) and capecitabine (4%). The primary endpoint in both studies was complete response (defined as no emetic episodes and no rescue medication) in the delayed phase (25 to 120 hours) of chemotherapy-induced nausea and vomiting.

Moderately Emetogenic Chemotherapy (MEC) and Combinations of Anthracycline and Cyclophosphamide Chemotherapy Study 3 In Study 3, a multicenter, randomized, double-blind, parallel group, controlled clinical study in moderately emetogenic chemotherapy, the VARUBI regimen (VARUBI, granisetron and dexamethasone) was compared with control therapy (placebo, granisetron and dexamethasone) in patients receiving a moderately emetogenic chemotherapy regimen that included at least 50% of patients receiving a combination of anthracycline and cyclophosphamide.

The percentage of patients who received carboplatin in Cycle 1 was 30%. Treatment regimens for the VARUBI and control arms are summarize… [Excerpted — this section continues on DailyMed.]

🧪 Nonclinical Toxicology ~1 min read ▾

13 NONCLINICAL TOXICOLOGY

13.1Carcinogenesis, Mutagenesis, Impairment of Fertility Carcinogenesis The carcinogenic potential of rolapitant was assessed in 2-year carcinogenicity studies in CD-1 mice and Sprague-Dawley rats. In mice, there were no drug-related neoplastic findings at doses up to 135 mg/kg per day (approximately 3.6 times the recommended human dose on a body surface area basis). In rats, there were no drug-related neoplastic findings at doses up to 90 mg/kg per day (approximately 4.9 times the recommended human dose on a body surface area basis).

Mutagenesis Rolapitant was not genotoxic in an Ames test, a human peripheral blood lymphocyte chromosome aberration test, and a mouse micronucleus test. Impairment of Fertility In a fertility and early embryonic development study in female rats, rolapitant at an oral dose of 9 mg/kg per day (approximately 0.5 times the recommended human dose on a body surface area basis) caused a transient decrease in maternal body weight gain and increases in the incidence of pre- and post-implantation loss. At a rolapitant dose of 4.5 mg/kg per day (approximately 0.2 times the recommended human dose on a body surface area basis), there were slight decreases in the number of corpora lutea and implantation sites.

Rolapitant did not affect the fertility or general reproductive performance of male rats at doses up to 90 mg/kg per day(approximately 4.9 times the recommended human dose on a body surface area basis). Reversibility in female rats was demonstrated in a follow-up study.

📄 Carcinogenesis, Mutagenesis, Impairment of Fertility ~1 min read ▾

13.1Carcinogenesis, Mutagenesis, Impairment of Fertility Carcinogenesis The carcinogenic potential of rolapitant was assessed in 2-year carcinogenicity studies in CD-1 mice and Sprague-Dawley rats. In mice, there were no drug-related neoplastic findings at doses up to 135 mg/kg per day (approximately 3.6 times the recommended human dose on a body surface area basis). In rats, there were no drug-related neoplastic findings at doses up to 90 mg/kg per day (approximately 4.9 times the recommended human dose on a body surface area basis).

Mutagenesis Rolapitant was not genotoxic in an Ames test, a human peripheral blood lymphocyte chromosome aberration test, and a mouse micronucleus test. Impairment of Fertility In a fertility and early embryonic development study in female rats, rolapitant at an oral dose of 9 mg/kg per day (approximately 0.5 times the recommended human dose on a body surface area basis) caused a transient decrease in maternal body weight gain and increases in the incidence of pre- and post-implantation loss. At a rolapitant dose of 4.5 mg/kg per day (approximately 0.2 times the recommended human dose on a body surface area basis), there were slight decreases in the number of corpora lutea and implantation sites.

Rolapitant did not affect the fertility or general reproductive performance of male rats at doses up to 90 mg/kg per day(approximately 4.9 times the recommended human dose on a body surface area basis). Reversibility in female rats was demonstrated in a follow-up study.

📄 Patient Package Insert ~3 min read ▾

This Patient Information has been approved by the U.S. Food and Drug Administration. Revised: 8/2026 PATIENT INFORMATION VARUBI ® (vuh ROO bee) (rolapitant) tablets, for oral use What is VARUBI?

VARUBI is a prescription medicine called an “antiemetic.” VARUBI is used with other medicines in adults to help prevent nausea and vomiting that happens later with certain anti-cancer medicines (chemotherapy). It is not known if VARUBI is safe and effective in children. Do not take VARUBI if you: take thioridazine or pimozide.

Taking VARUBI with thioridazine or pimozide can cause serious or life-threatening heart rhythm changes. are a child less than 2 years of age. Before taking VARUBI, tell your doctor about all of your medical conditions, including if you: have liver problems. are pregnant or plan to become pregnant. It is not known if VARUBI will harm your unborn baby.

VARUBI may affect the ability to have a child (fertility problems) in females. are breastfeeding or plan to breastfeed. It is not known if VARUBI passes into your breast milk or could harm your baby. Talk to your doctor about the best way to feed your baby if you take VARUBI.

Tell your doctor about all the medicines you take or stop taking , including prescription and over-the-counter medicines, vitamins, and herbal supplements. Keep a list of your medicines to show your doctor and pharmacist when you get a new medicine. VARUBI and other medicines may affect each other and could cause serious side effects.

How should I take VARUBI? Take VARUBI exactly as your doctor tells you to take it. VARUBI is taken on Day 1 of chemotherapy.

Take 2 VARUBI tablets by mouth within 2 hours before you receive your anti-cancer medicine (chemotherapy). VARUBI can be taken with or without food. Do not take VARUBI more than 1 time every 14 days.

If you take too much VARUBI, call your doctor or go to the nearest hospital emergency room right away. What are the possible side effects of VARUBI? VARUBI may cause serious side effects, including: Change in the level of some medicines in your blood.

Serious or life-threatening reactions, including heart rhythm changes, may occur if VARUBI is used with certain other medicines. You should not take VARUBI if you take thioridazine or pimozide. The most common side effects of VARUBI in people who take VARUBI and receive Cisplatin chemotherapy medicine include : low white blood cell count, hiccups, and stomach (abdominal) pain.

The most common side effects of VARUBI in people who take VARUBI and receive Anthracycline and Cyclophosphamide chemotherapy medicines include: decreased appetite, low white blood cell count, dizziness, indigestion, urinary tract infection, mouth sores, and low red blood cell count. These are not all the possible side effects of VARUBI. Call your doctor for medical advice about side effects.

You may report side effects to FDA at 1-800-FDA-1088. How should I store VARUBI? VARUBI comes in a child-resistant package.

Store VARUBI at room temperature between 68°F to 77°F (20°C to 25°C). Keep VARUBI and all medicines out of the reach of children. General information about the safe and effective use of VARUBI.

Medicines are sometimes prescribed for purposes other than those listed in a Patient Information leaflet. Do not use VARUBI for a condition for which it was not prescribed. Do not give VARUBI to other people, even if they have the same symptoms that you have.

It may harm them. You can ask your doctor or pharmacist for information about VARUBI that is written for health professionals. What are the ingredients in VARUBI?

Active ingredient: rolapitant Inactive ingredients: colloidal silicon dioxide, croscarmellose sodium, lactose monohydrate, magnesium stearate, microcrystalline cellulose, povidone, and pregelatinized starch. The tablets are coated in non-functional blue and clear coats. The tablet coating comprises the following inactive ingredients: FD&C Blue No.

2-Indigo Carmine Lake, polyethylene glycol, polysorbate 80, polyvi… [Excerpted — this section continues on DailyMed.]

📄 Package Label / Principal Display Panel 121 words ▾

PRINCIPAL DISPLAY PANEL - 90 mg Tablet Blister Wallet NDC 87628-101-02 Single dose 180 mg total dose (2 x 90 mg tablets) VARUBI ® (rolapitant) tablets 90 mg* per tablet Contains two 90 mg tablets equal to a single dose of 180 mg *(equivalent to 100 mg rolapitant hydrochloride) Rx only For oral use. Keep this and all drugs out of the reach of children. This package is child-resistant.

Store at 20°C - 25°C (68°F - 77°F); excursions permitted to 15°C - 30°C (59°F - 86°F) [see USP Controlled Room Temperature]. LURIA Distributed by: Luria Therapeutics LLC, Pleasant Prairie, WI 53158 See package insert for dosage information. Figure

PRINCIPAL DISPLAY PANEL - NDC: 87628-101-02 - Blister Backing Label Blister Backing Label

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

Medicare Part D spend CMS · PART D · 2026 (Q1)

Medicare Part D (outpatient prescription) spending for Varubi — the program that covers self-administered drugs. 1 manufacturer.
⚠️ Drug-level data: CMS publishes Part D spending by drug, not by NDC — these figures combine every manufacturer, strength and package size sold under the name Varubi. That’s a different level of aggregation than the Medicaid card above, which is specific to this exact 11-digit NDC (pack size included), so the two aren’t directly comparable.
Period
Total Part D spend
$75.9K
Claims incl. refills
84
Beneficiaries
44
Spend / beneficiary
$1,724.19
Spend / claim
$903.15
Trend by period
💵 About the dollar figures: spending is what Part D plans paid before confidential manufacturer rebates, so the program’s real net cost is lower. A blank patient count means fewer than 11 people — CMS hides counts that small to protect privacy. Source: CMS Medicare Quarterly Part D Spending by Drug (data.cms.gov), updated quarterly.

Reported adverse events (FAERS)

Read carefully: FAERS reports are voluntary and unverified. Counts are not incidence, do not establish causation, are subject to reporting bias, and cannot be used to compare one drug to another. Shown for signal context only. Reports for Varubi (this brand).

Top reported reactions

Death143
Nausea79
Fatigue51
Infusion Related Reaction40
Dyspnoea34
Decreased Appetite33
Flushing32

Age at onset

Adult4
Elderly9

Reporter sex

538 reports
Male · 43%
Female · 57%

Serious outcomes

Death163
Hospitalization115
Life-threatening11
Disabling1
Reports over time (by year) — tap or hover for the count & year
2019 2021 2023 2026 116 3
Most recent year is provisional (FAERS lags ~3 months).
Where does this data come from?
Adverse-event reports from the FDA Adverse Event Reporting System (FAERS) via openFDA. FAERS reports are voluntary and unverified — counts are not incidence and don’t establish causation.

About this NDC listing & data coverage

Finished prescription product
What data is (and isn’t) available for this NDC — tap to expand
NDC identity (package / product / labeler codes) ✓ Available
Labeler ✓ Available
Product & package description ✓ Available
Marketing category & status ✓ Available
Active ingredient / dosage form / route ✓ Available
FDA label (SPL via DailyMed) ✓ Available
Package photos ✓ Available
Inactive ingredients (structured) ✓ Available
NADAC pharmacy acquisition price (CMS) — Not published for this NDC CMS publishes NADAC only for NDCs reported in its retail-pharmacy survey.
Orange Book / therapeutic-equivalence data ✓ Available
HCPCS J-code billing crosswalk — Not published for this NDC Most self-administered / retail products have no J-code — that is normal.
Medicaid utilization (CMS SDUD) — Not published for this NDC CMS reports utilization only for NDCs with Medicaid claims above its privacy threshold.
“Not published” reflects what the public FDA / CMS / NLM sources provide for this exact package code — it is a property of the data feeds, not a judgment about the product.

Questions about this listing

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.
Is the NDC printed on the package the same as the 11-digit billing NDC?
Yes, they identify this exact package in different formats. The form printed on the packaging and shown on DailyMed is the one the FDA registered. Insurance claims use a fixed 11-digit 5-4-2 format, so the short segment is padded with a leading zero and the dashes are dropped. The Identity section at the top of this page lists each form of this code.
Is this package still being marketed?
Yes, per the latest FDA NDC Directory data on this page: this package is listed as actively marketed, with no marketing end date reported by Luria Therapeutics LLC. Listing status can change — the directory data on this page refreshes weekly.
Who lists this product with the FDA?
Luria Therapeutics LLC is the labeler of record for this NDC — the company under whose FDA-assigned code the package is listed. The labeler may be the manufacturer itself or a distributor marketing the product under its own code.
Do I need a prescription for this product?
This NDC is listed with FDA as a prescription product, so it is dispensed under a prescriber's order. Your pharmacist can tell you whether any over-the-counter forms of the same medication exist.
This page identifies an FDA-listed package (the NDC) and reports public regulatory and pricing data about the listing. It is reference information, not a medical recommendation — talk to your pharmacist or prescriber about your own medication.
Where does this data come from?
Listing facts (marketing category, packager status, marketing dates) from the FDA openFDA NDC Directory; label availability from DailyMed; pricing coverage from CMS NADAC; equivalence scope from the FDA Orange Book.
← 87627-0001-00 · King-Tech 87630-0101-11 · Sichuan →
For educational and professional reference only — not medical advice. Pricing reflects published NADAC and CMS ASP (free public data) and may differ from your acquisition cost; always verify before billing or dispensing.