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Pharmacology Drug Notes - Katzung-Based

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1. EZETIMIBE (Cholesterol Absorption Inhibitor)

• Undergoes glucuronidation in the small intestine and liver
• Enters enterohepatic recirculation - this prolongs its effect
• Half-life: ~22 hours - allows once-daily dosing
• Negligible systemic exposure due to first-pass glucuronidation
• Dose: 10 mg once daily

• Reduces LDL-C by ~18-20% as monotherapy
• Minimal effect on TG or HDL-C
• Complementary mechanism to statins and bempedoic acid (ACL inhibitor)
• Combination with statin gives additive LDL lowering

• Primary hypercholesterolemia (adjunct to statin or monotherapy in statin-intolerant patients)
• Familial hypercholesterolemia (combined with statin)
• SHARP trial: simvastatin + ezetimibe → 17% reduction in major vascular events in CKD patients

• Very well tolerated
• Hepatotoxicity risk nearly identical to placebo (0.5% vs 0.3%)
• No documented increased myopathy risk
• Rare: diarrhea, arthralgia

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2. NIACIN (Nicotinic Acid) / "Minti Wagwlanl" - interpreted as Niacin/Niacin-like agent

• Acts on the GPR109A receptor (G-protein coupled) on adipocytes → inhibits adipose tissue hormone-sensitive lipase → reduces free fatty acid (FFA) flux to the liver → decreases hepatic VLDL and TG synthesis
• Reduces LDL by reducing VLDL precursor supply
• Increases HDL by reducing HDL apolipoprotein (apoA-I) catabolism

• Lowers TG most effectively (20-50%)
• Raises HDL by 20-35% (most effective agent)
• Lowers LDL by 10-20%
• Lowers Lp(a)

• Hypertriglyceridemia, mixed dyslipidemia
• In combination for comprehensive lipid management

• Flushing (most common) - prostaglandin-mediated; reduced by aspirin pretreatment or extended-release formulation
• Pruritus
• Hyperglycemia - worsen insulin resistance
• Hyperuricemia - can precipitate gout
• Hepatotoxicity - particularly with sustained-release forms
• GI upset, peptic ulcer exacerbation
• Acanthosis nigricans (skin thickening)

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3. RIVAROXABAN (Factor Xa Inhibitor)

• Oral bioavailability: ~66% fasting, ~80-100% with food - must be taken WITH food at doses ≥15 mg
• Maximum absorption occurs in the stomach; tablet can be crushed for NG tube delivery
• Dual elimination: ~2/3 hepatic (CYP3A4 and CYP2J2), ~1/3 renal unchanged
• Half-life: 5-9 hours (healthy adults), 11-13 hours (elderly)
• Substrate of P-glycoprotein - P-gp inhibitors (e.g., verapamil) increase drug levels

• Combined P-gp and CYP3A4 inhibitors (ketoconazole, ritonavir) → significantly increase plasma levels → avoid
• CYP3A4 inducers (rifampin, phenytoin) → reduce efficacy

• Nonvalvular atrial fibrillation (stroke prevention)
• DVT/PE treatment and prevention
• Post-surgical VTE prophylaxis (hip/knee arthroplasty)
• Post-ACS (2.5 mg BID + aspirin, COMPASS trial)
• PAD revascularization (VOYAGER PAD trial: 2.5 mg BID + ASA 81 mg)
• Extended VTE prophylaxis in high-risk medical patients (10 mg/day x 45 days post-discharge)

• Bleeding (most important) - no specific antidote historically; andexanet alfa is now approved reversal agent
• Major bleeding higher than enoxaparin in some surgical VTE trials
• No need for routine INR monitoring

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4. CLOPIDOGREL / ASPIRIN (Antiplatelet Agents)

Clopidogrel

• Oral prodrug: ~50% absorbed, undergoes 2-step hepatic oxidation via CYP1A2, CYP2C19 (main), CYP3A4
• Loading dose: 300-600 mg (rapid effect in 2-3 hours with 600 mg)
• Maintenance: 75 mg/day (steady-state platelet inhibition in ~3-5 days)

• PPIs (especially omeprazole, esomeprazole): inhibit CYP2C19 → reduce active metabolite formation → reduced antiplatelet effect (clinical significance debated)
• Atorvastatin (CYP3A4 competitor): may reduce efficacy
• Opioids: delay absorption of active metabolite
• CYP2C19 poor metabolizers (genetic polymorphism): reduced conversion → "clopidogrel resistance" → consider prasugrel or ticagrelor

• ACS (NSTEMI, STEMI) - dual antiplatelet therapy (DAPT) with aspirin
• Post-PCI
• Ischemic stroke / TIA
• Peripheral arterial disease
• CAPRIE trial: clopidogrel superior to aspirin in reducing ischemic stroke, MI, and vascular death

• Bleeding (especially GI)
• TTP (rare but serious)
• Neutropenia (rare)

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Aspirin (Acetylsalicylic Acid)

• Primary and secondary CV prevention
• ACS, post-MI, post-PCI (as part of DAPT)
• Ischemic stroke
• Kawasaki disease (anti-inflammatory doses)
• Pre-eclampsia prophylaxis (low-dose)

• GI irritation, peptic ulcers, GI bleeding
• Reye's syndrome (children + viral illness)
• Bronchospasm (aspirin-exacerbated respiratory disease)
• Prolonged bleeding time
• Tinnitus / salicylism at high doses

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5. RANOLAZINE

• Reduces intracellular Ca²+ overload
• Improves diastolic relaxation
• Reduces myocardial oxygen demand
• Also has beta-cell glucose-dependent insulin secretion benefit (minor)

• Oral bioavailability: ~75%
• Extensively metabolized by CYP3A4 (major) and CYP2D6
• Half-life: ~7 hours (but extended-release formulation → BID dosing)
• Substrate of P-glycoprotein (P-gp) - P-gp inhibitors (digoxin, cyclosporine) can increase exposure
• Dose: 500-1000 mg BID (extended-release)

• Strong CYP3A4 inhibitors (ketoconazole, clarithromycin, HIV protease inhibitors, diltiazem, verapamil): significantly increase ranolazine levels → contraindicated or reduce dose
• CYP3A4 inducers (rifampin, carbamazepine): decrease levels → avoid
• QT prolongation risk: avoid with other QT-prolonging drugs (quetiapine, etc.)
• Simvastatin interaction: ranolazine inhibits CYP3A4 → increases simvastatin exposure (avoid co-use per Washington Manual)

• Chronic stable angina refractory to standard therapy (nitrates, beta-blockers, CCBs)
• Can substitute for beta-blockers in intolerant patients
• Does NOT reduce mortality

• QTc prolongation (dose-dependent)
• Constipation, nausea, dizziness
• Headache

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6. SILDENAFIL (PDE5 Inhibitor)

• Oral bioavailability: ~40% (high first-pass)
• Onset: within 30-60 min
• Duration: ~4 hours
• Metabolized by CYP3A4 (major) and CYP2C9 (minor)
• Food (especially high-fat meals) delays absorption and reduces Cmax
• Dose: 50 mg 1 hour before intercourse (range 25-100 mg)
• For pulmonary arterial hypertension (PAH): 20 mg TID

• Nitrates (ABSOLUTE CONTRAINDICATION) - both drugs lower blood pressure via cGMP pathway → severe, potentially fatal hypotension
• Alpha-blockers (terazosin, tamsulosin): additive hypotension - use caution
• CYP3A4 inhibitors (ketoconazole, erythromycin, ritonavir, cimetidine): increase sildenafil levels
• CYP3A4 inducers (rifampin, bosentan): decrease levels substantially

• Erectile dysfunction (ED)
• Pulmonary arterial hypertension (PAH) - as Revatio
• Raynaud phenomenon (off-label)
• High-altitude pulmonary edema prevention (off-label)
• May reverse SSRI-induced anorgasmia/sexual dysfunction

• Headache, flushing, dyspepsia (most common)
• Nasal congestion
• Blue-tinted vision (cyanopsia) - PDE6 inhibition in retina
• Priapism (rare)
• Sudden hearing loss (rare)
• Hypotension - particularly with nitrates or alpha-blockers

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7. BETA-2 AGONISTS

• Onset: 5-15 min, Duration: 4-6 hours
• Used for: acute bronchospasm rescue, exercise-induced bronchospasm

• Salmeterol: onset 15-30 min, Duration: 12 hours
• Formoterol: onset 5-15 min, Duration: 12 hours (faster onset than salmeterol)
• Indacaterol: once-daily LABA (COPD only in US)
• Used for: maintenance therapy in asthma (must be combined with ICS) and COPD

• Inhaled route preferred (topical effect, reduced systemic side effects)
• Regular use → receptor downregulation/tolerance (tachyphylaxis) to both bronchodilator and non-bronchodilator effects

• Tremor (skeletal muscle β2 effect) - most common
• Tachycardia, palpitations (β1 spillover)
• Hypokalemia (K+ shift into cells via β2-Na+/K+ATPase)
• Hypoxemia (mild) in severe COPD - via pulmonary vasodilation, increased V/Q mismatch
• Metabolic effects: hyperglycemia, lactic acidosis (high doses)
• Tolerance with regular use

• Asthma (SABA: rescue; LABA + ICS: maintenance)
• COPD (SABA/LABA: both for symptom control)
• Hyperkalemia (albuterol IV/nebulized as temporizing measure)
• Premature labor (terbutaline, but not recommended for prolonged use)

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8. LAMA - Long-Acting Muscarinic Antagonist

• M3 blockade → prevents acetylcholine-mediated bronchoconstriction → bronchodilation
• M1 blockade → reduces parasympathetic ganglionic transmission
• M2 receptors on presynaptic nerve terminals (autoreceptors) are also blocked, which can paradoxically increase ACh release - but net effect is bronchodilation

• COPD (first-line) - reduces exacerbations, improves lung function and quality of life
• Asthma (adjunct in severe/uncontrolled asthma)
• Most effective bronchodilator class for COPD

• Dry mouth (most common)
• Urinary retention
• Constipation
• Blurred vision, acute angle-closure glaucoma (if inhaled drug contacts eyes)
• Tachycardia (M2 block on SA node)
• Paradoxical bronchospasm (rare)

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9. LABA (Long-Acting Beta-2 Agonist)

• Salmeterol: extrinsic pathway - long alkyl chain anchors to receptor exosite → sustained bronchodilation
• Formoterol: intrinsic pathway - high lipophilicity → partitions into membrane → sustained release

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10. INSULIN (and Hypoglycemics)

• Liver: ↑ glycogen synthesis, ↑ lipogenesis, ↓ gluconeogenesis, ↓ glycogenolysis
• Muscle: ↑ glucose uptake (GLUT4), ↑ protein synthesis
• Adipose: ↑ lipogenesis, ↓ lipolysis (most sensitive to anti-lipolytic effect)
• Potassium shift: ↑ K+ uptake (used to treat hyperkalemia)

• Hypoglycemia - most important
• Weight gain
• Lipodystrophy at injection sites
• Hypokalemia
• Allergic reactions (rare with human insulin)

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11. PPAR-GAMMA AGONISTS (Thiazolidinediones / TZDs)

• Promotes adipocyte differentiation (small, insulin-sensitive adipocytes over large resistant ones)
• Increases GLUT4 and GLUT1 gene expression
• Increases adiponectin secretion (sensitizes liver and muscle to insulin)
• Reduces free fatty acid release from adipocytes
• Net effect: reduces insulin resistance in muscle, liver, and adipose

• Type 2 diabetes mellitus
• NASH/NAFLD (pioglitazone shows histological improvement)
• Polycystic ovary syndrome (PCOS) - improve insulin sensitivity

• Weight gain (fat redistribution, fluid retention)
• Edema - fluid retention via increased renal sodium reabsorption
• Heart failure exacerbation - contraindicated in NYHA Class III-IV HF
• Bone fractures - increased risk especially in women (distal limb fractures)
• Macular edema (rare)
• Rosiglitazone: increased risk of myocardial infarction (controversial; FDA restricted use - currently lifted)
• Pioglitazone: possible small increased risk of bladder cancer (prolonged use)
• Hepatotoxicity (troglitazone - withdrawn; not significant with current drugs)

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12. DPP-4 INHIBITORS (Gliptins)

• GLP-1 (glucagon-like peptide-1): glucose-dependent insulin secretion, suppresses glucagon, delays gastric emptying
• GIP (glucose-dependent insulinotropic polypeptide): stimulates insulin secretion

• Sitagliptin: primarily renally excreted → dose-reduce in CKD
• Linagliptin: biliary/fecal excretion → no dose adjustment needed in renal failure (most convenient in CKD)
• Saxagliptin: CYP3A4 metabolized

• Generally very well tolerated
• Nasopharyngitis, upper respiratory tract infections (most common)
• Pancreatitis (rare but black box concern)
• Joint pain / arthralgia
• Saxagliptin, alogliptin: increased risk of hospitalization for heart failure (FDA warning) - avoid in HF with reduced EF

• Type 2 diabetes (monotherapy or combination)
• Particularly useful in elderly and CKD patients (especially linagliptin)

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13. METHIMAZOLE

1. Oxidation of iodide to active iodine
2. Organification - incorporation of iodine into thyroglobulin tyrosine residues
3. Coupling of iodotyrosines (MIT + DIT) to form T3 and T4

• Well absorbed orally
• Concentrated in thyroid tissue
• Half-life: ~4-6 hours but intrathyroidal concentration allows once-daily dosing at low doses
• Dose: 10-40 mg/day, can be once or divided

• Drug of choice for hyperthyroidism / Graves' disease (except exceptions below)
• Preparation for thyroidectomy or radioiodine therapy
• Thyroid storm (combined with iodine, steroids, beta-blockers)

• First trimester of pregnancy (methimazole teratogenic - aplasia cutis, choanal atresia)
• Thyroid storm (for T4→T3 conversion block)
• Adverse reactions to methimazole

• Agranulocytosis - most serious (0.2-0.5%) - warn patients to seek immediate care for fever/sore throat
• Rash, urticaria
• Arthralgia, arthralgias ("lupus-like")
• Cholestatic jaundice
• Hypothyroidism (if overtreated)
• Teratogenic: aplasia cutis, choanal atresia, esophageal atresia (contraindicated in 1st trimester)

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14. MIFEPRISTONE (RU-486)

1. Competitively antagonizes progesterone receptors (PR-A and PR-B) with higher affinity than progesterone itself
2. Also antagonizes glucocorticoid receptors (GR) (weaker affinity, but clinically relevant at high doses)

• Oral bioavailability: ~70%
• Highly protein-bound (albumin, alpha-acid glycoprotein)
• Metabolized by CYP3A4
• Long half-life: ~18-20 hours (allows single-dose regimens)
• Dose for medical abortion: 200 mg mifepristone followed 24-48 hours later by 800 mcg misoprostol (PGE1 analog)

1. Medical abortion (up to 70 days gestation) - combined with misoprostol; ~95-99% effective
2. Emergency contraception (single 10 mg dose)
3. Cushing's syndrome (Korlym - 300-1200 mg/day; blocks GR to reduce hypercortisolism effects in glucose intolerance)
4. Endometriosis, uterine fibroids (investigational)
5. Meningiomas and breast cancers expressing GR/PR (investigational)

• Uterine cramping, heavy bleeding (expected therapeutic effects)
• Nausea, vomiting, diarrhea
• Incomplete abortion (requires surgical completion ~1-5%)
• Infection (rare; serious Clostridium sordellii cases with vaginal misoprostol)
• Adrenal insufficiency risk at high doses (anti-glucocorticoid effect)

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15. ALPHA-GLUCOSIDASE INHIBITORS

• Must be taken with first bite of each main meal
• Acarbose: minimally absorbed systemically (local gut action)
• Miglitol: completely absorbed but excreted unchanged by kidneys
• Dose: Acarbose 25-100 mg TID with meals; gradually uptitrate

• Type 2 diabetes (adjunct or monotherapy, especially for postprandial hyperglycemia)
• Impaired glucose tolerance / prediabetes prevention
• Low hypoglycemia risk as monotherapy

• GI symptoms are the major limitation: flatulence, bloating, abdominal cramps, diarrhea
• These are caused by undigested carbohydrates reaching the colon → fermented by bacteria → gas production
• Hepatotoxicity (rare, mainly with acarbose at doses >300 mg/day)
• Anemia (rare)

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16. PIOGLITAZONE

• Pioglitazone: ↓ TG, ↑ HDL, LDL effect variable (shifts to larger, less atherogenic LDL particles) - net favorable lipid profile
• Rosiglitazone: ↑ LDL (less favorable) - restricted by FDA

• PROactive trial: pioglitazone reduced secondary CV endpoints in T2DM patients with established CVD (not primary endpoint)
• No FDA indication for CV protection, but no CV harm demonstrated

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17. METOLAZONE

• Long half-life: ~14 hours → once-daily dosing
• Dose: 2.5-10 mg daily (may use intermittently - 2-3x/week in chronic HF)

• Hypertension (especially with renal impairment)
• Diuretic resistance in heart failure - commonly added to loop diuretics (furosemide/bumetanide) for synergistic diuresis ("sequential nephron blockade")
• Nephrotic syndrome

• Hypokalemia (most common electrolyte issue) - watch when combined with loop diuretics
• Hyponatremia (dilutional)
• Hyperuricemia / gout
• Hyperglycemia (impairs insulin secretion)
• Hypercalcemia (unlike loop diuretics)
• Hypomagnesemia
• Hyperlipidemia (mild)
• Photosensitivity

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18. LMWH (Low Molecular Weight Heparin)

• Predictable pharmacokinetics (fixed-weight-based dosing)
• No need for aPTT monitoring (exception: renal failure, obesity, pregnancy)
• Subcutaneous administration with ~90% bioavailability
• Renal elimination (dose-reduce in CrCl <30) - risk of accumulation
• Half-life: ~4-6 hours

• DVT/PE treatment and prophylaxis
• ACS (NSTEMI/STEMI) - enoxaparin
• Bridging anticoagulation
• VTE prophylaxis post-surgery
• Anticoagulation in pregnancy (safe, does not cross placenta)

• Bleeding
• HIT (Heparin-Induced Thrombocytopenia) - much lower incidence than UFH (~0.1% vs 1-3%)
• Osteoporosis (with prolonged use)
• Injection site reactions (bruising)

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19. UFH (Unfractionated Heparin)

• Thrombin (Factor IIa) - requires simultaneous binding of heparin to AT-III and thrombin (requires chain length ≥18 saccharides)
• Factor Xa - only AT-III binding required

• IV or SC administration (IV for acute anticoagulation; SC for prophylaxis)
• Variable pharmacokinetics (binds plasma proteins, endothelium, macrophages) → unpredictable dose-response
• Monitoring: aPTT (target 60-100 seconds = 1.5-2.5x normal) or anti-Xa levels
• Half-life: dose-dependent (~30-90 min IV)

• Fully reversible with protamine
• Can use in severe renal failure (not renally cleared)
• IV titration allows precise real-time adjustment (e.g., cardiopulmonary bypass, ECMO)

• Acute VTE treatment (DVT/PE)
• ACS (NSTEMI/STEMI - IV infusion)
• Mechanical heart valves (bridging)
• Cardiopulmonary bypass
• Intraoperative anticoagulation

• Bleeding
• HIT (Heparin-Induced Thrombocytopenia) - 1-3%; Type II HIT is an immune-mediated thrombocytopenia with paradoxical THROMBOSIS (HIT-T). Caused by antibodies against heparin-PF4 complex → platelet activation → thrombosis. Treat by stopping heparin immediately and starting a direct thrombin inhibitor (argatroban, bivalirudin).
• Osteoporosis (long-term use)
• Hypoaldosteronism → hyperkalemia (long-term use)
• Elevated liver transaminases

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20. BETA-BLOCKERS

• Heart: ↓ HR (chronotropy), ↓ contractility (inotropy), ↓ conduction velocity (dromotropy)
• Kidney: ↓ renin secretion → ↓ angiotensin II → ↓ aldosterone → blood pressure reduction
• Lungs (nonselective): β2 blockade → bronchospasm
• Metabolic: Masks tachycardia of hypoglycemia; impairs glycogenolysis (prolonged hypoglycemia); ↓ HDL, ↑ TG; ↑ K+ (blocking β2-mediated K+ uptake)

• Hypertension
• Heart failure with reduced EF (HFrEF) - carvedilol, metoprolol succinate, bisoprolol (mortality benefit proven)
• Ischemic heart disease/angina - ↓ myocardial O2 demand
• ACS (post-MI) - reduce mortality
• Arrhythmias - AF rate control, SVT, ventricular arrhythmias
• Hyperthyroidism/thyroid storm (symptom control - propranolol; also blocks T4→T3 conversion)
• Pheochromocytoma (ONLY after adequate alpha-blockade to prevent hypertensive crisis)
• Essential tremor (propranolol)
• Migraine prophylaxis (propranolol, metoprolol)
• Portal hypertension / varices (propranolol, nadolol)
• Anxiety (propranolol - situational)

• Bradycardia, heart block
• Acute HF decompensation (if started during acute decompensation)
• Bronchospasm (avoid nonselective in asthma/COPD)
• Fatigue, cold extremities, sexual dysfunction
• Rebound hypertension/angina if abruptly discontinued - always taper
• Metabolic: hyperglycemia (masks symptoms), hypertriglyceridemia, ↓HDL
• Depression (CNS-penetrant drugs: propranolol)

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21. FIBRATES (Fibric Acid Derivatives)

1. Increases lipoprotein lipase (LPL) → enhanced clearance of TG-rich VLDL and chylomicrons → ↓ TG
2. Reduces apoC-III (an LPL inhibitor) → further enhances VLDL clearance
3. Increases apoA-I and apoA-II synthesis → ↑ HDL
4. Reduces hepatic fatty acid synthesis
5. Promotes fatty acid beta-oxidation

• ↓ Triglycerides: 20-50% (primary effect - most powerful oral TG-lowering agents)
• ↑ HDL: 10-20%
• LDL effect variable (may ↑ LDL-C as VLDL converts to LDL; fenofibrate shifts to larger LDL)

• Gemfibrozil and fenofibrate: well absorbed orally (food increases absorption)
• Fenofibrate is a prodrug → hydrolyzed to fenofibric acid
• Fenofibrate: extensive renal clearance → dose reduction in renal impairment
• Gemfibrozil: hepatic metabolism (no renal adjustment needed)
• Gemfibrozil is more likely to cause statin myopathy (inhibits statin glucuronidation → ↑ statin levels)

• Severe hypertriglyceridemia (TG >500 mg/dL to prevent pancreatitis) - primary indication
• Mixed dyslipidemia
• NOT established for primary ASCVD event reduction (unlike statins); guidelines recommend only for severe TG reduction
• Fenofibrate not superior to gemfibrozil for primary CV endpoint in most trials

• Myopathy/rhabdomyolysis - especially when combined with statins (gemfibrozil > fenofibrate with statin risk)
• Cholelithiasis - fibrates increase biliary cholesterol secretion → gallstones
• GI disturbances
• Elevated liver transaminases
• Elevated serum creatinine (fenofibrate, bezafibrate, ciprofibrate - in cyclosporine-treated patients)
• Venous thromboembolism (slight increase noted in some studies)

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Summary Table

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• "Minti wagwlanl" - interpreted as Niacin (the classic "flushing" drug; if you meant something else, let me know)
• "Unsulin = au hypes" - interpreted as Insulin and hypoglycemics (insulin types covered)
• "Sindenafil" = Sildenafil (covered)
• "Cropidogrel" = Clopidogrel (covered)

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1. Ezetimibe works at NPC1L1 (brush border); undergoes enterohepatic recirculation; 20% LDL reduction
2. Rivaroxaban MUST be taken with food at therapeutic doses (≥15 mg); anti-Xa activity monitored when needed
3. Clopidogrel is a prodrug requiring CYP2C19 - PPIs reduce its activation; genetic polymorphisms cause "resistance"
4. Ranolazine blocks late INa (not HR/BP) - unique mechanism; QTc prolongation risk; CYP3A4 substrate
5. Sildenafil + nitrates = ABSOLUTE contraindication (fatal hypotension via dual cGMP elevation)
6. LABAs must NEVER be used without ICS in asthma
7. LAMA (tiotropium) is the cornerstone bronchodilator in COPD
8. DPP-4 inhibitors are glucose-dependent → very low hypoglycemia risk; linagliptin needs no renal dose adjustment
9. Methimazole is preferred over PTU except in first trimester, thyroid storm, and PTU-intolerance
10. Mifepristone blocks both PR and GR; used for medical abortion AND Cushing's syndrome
11. Metolazone works in renal failure (unlike HCTZ) - synergizes powerfully with loop diuretics
12. UFH preferred over LMWH in severe renal failure and when rapid reversal is needed (protamine fully reverses)
13. HIT - stop ALL heparin (UFH and LMWH) immediately; switch to direct thrombin inhibitor (argatroban)
14. Fibrates activate PPARα (not PPARγ) - primary use is severe hypertriglyceridemia; avoid gemfibrozil + statin combination