New drugs approved 2025-2026

Hinzugefügt: 2026-05-20

[00:00:07]Hello guys. So, welcome to this year edition of learning the new drugs which are approved. So, in this version three, we will be discussing the newly approved drugs which are important for you from May 2025 to 2026.

[00:00:23]Now, what about the previously approved drugs? You can check the older version, version one, in which we have discussed the drugs approved till 2023.

[00:00:34]And the version two, in which we have discussed the drug approved for from November 2023 to 2025, which are previously uploaded in this YouTube channel of Dr. Ankit Pharmacology Series.

[00:00:47]And in this section, we will start from the drugs from May 2025 to 2026, 1-year newly approved drug.

[00:00:56]So, for more updates, you can join and the this YouTube channel. The link is given. And you can also follow on Instagram for regular updates. So, let's learn the newly approved drugs. And besides the newly approved drug, I will be telling you the previous standard therapy as well, which is already approved for a disease.

[00:01:17]So, the first, let's start with the drugs approved for endocrine system in diabetes mellitus. The first new, newly approved insulin is insulin icodec.

[00:01:29]Now, remember till now, insulin degludec was the longest-acting insulin. It used to act for 42 hours.

[00:01:38]And before degludec, there was insulin glargine, which used to act for 24 hours. And these two insulins are known as basal insulin.

[00:01:49]But now, we have a new insulin in the market, that is insulin icodec. And insulin ecodeck act for 196 hours. So, it's a new basal insulin recently approved and now insulin ecodeck is considered to be the overall longest acting insulin in the market.

[00:02:13]Now, another drug approved for diabetes as well as obesity. Earlier, it was approved for diabetes mellitus, but this drug was causing weight loss. So, the drug is or for gliptron and this drug has been approved for obesity. So, how we can remember? Or means it's an oral drug and you can see the word glip. G L I P word is coming. GLP stands for glucagon-like peptide. Glucagon-like peptide one. So, that is why glip word is coming and glucagon-like peptide causes weight loss because it suppresses appetite. So, if you will not eat anything, obviously, there will be weight loss, but apart from this, what are the other options we have for obesity? We can make a mnemonic list. We can make a mnemonic list where L I stands for liraglutide. It is given by injections.

[00:03:18]We have semaglutide given by injection, but now it is also available orally and it comes with a brand name Ozempic. So, with Ozempic, now your ears, they have stood up that it is a very famous drug for promoting weight loss for the treatment of obesity. And we have tirzepatide. It is also an injectable drug. So, they are also similar glucagon-like peptide agonist, but what is a good thing about orforgliptron?

[00:03:48]Instead of injection, it is an oral drug we have for treatment of obesity. Now remember liraglutide, it causes approximately 10% weight loss.

[00:04:01]Orlistat, forglipron, it causes 12.5% weight loss.

[00:04:07]Semaglutide causes approximately 15% weight loss. And tirzepatide, which is even more effective drug, it causes around 20% of weight loss. So the most effective drug for weight loss now is tirzepatide.

[00:04:23]Next question.

[00:04:25]Paltusotine for acromegaly. Now paltusotine, it acts on pituitary.

[00:04:33]And on pituitary, it stimulates somatostatin receptor. And we know somatostatin is a inhibitory hormone. So it stimulates somatostatin type 2 receptor, which will decrease the production of growth hormone. So what happens in acromegaly? In acromegaly, there is excess of growth hormone. So for the treatment of acromegaly, we have to reduce growth hormone production. Now remember the first drug of choice for the treatment of acromegaly, we can give synthetic form of somatostatin. And these drugs, they end with the word reotide. They are the first drug of choice for the treatment of acromegaly.

[00:05:18]Octreotide, lanreotide, they are given by injection. In octreotide and lanreotide resistant cases, we have a drug pegvisomant for the treatment of acromegaly. Pegvisomant is not a somatostatin. It does not reduce the production of growth hormone.

[00:05:37]It is a rather A N T word is coming and soma word is coming. Soma means growth hormone. A N T means it rather block the receptor of growth hormone. So, it is a growth hormone receptor antagonist, and pegvisomant, it is also given by injection. Now, in pegvisomant resistant cases, we have a new drug paltu sotine.

[00:06:03]And the good thing with paltusotine is it's an oral drug, so it is the only oral available option for the treatment of acromegaly. Now, the next question we have Next drug is naevi pegritide and vosoritide.

[00:06:20]So, you can see both these drugs are ending with a word ritide.

[00:06:24]Okay? And these drugs, the ritide drugs, they are the synthetic form of C-type of natriuretic peptide.

[00:06:35]So, these drugs, they're ending with a word ritide. Remember, tide means it's a peptide, so it's a CNP. Now, what is the function of C-type of natriuretic peptide? C-type of natriuretic peptide inhibit the production of one protein known as FGF21 23. FGF stands for fibroblast growth factor 23. And this fibroblast growth factor 23 causes stoppage of bone growth. It causes stoppage of bone bone growth, so the person will become very short height. This short height is known as achondroplasia.

[00:07:17]It leads to premature closure of epiphysis, which leads to achondroplasia. So, we inhibit fibroblast growth factor by giving C-type of natriuretic peptide given for achondroplasia. But if we recall, there is another drug, nesiritide.

[00:07:37]Another drug which is ending with a word ritide is nesiritide. Nesiritide is rather BNP. It is not CNP, it is B type of natriuretic peptide and nesiritide is rather given in the patient of heart failure.

[00:07:54]Or you can write acute heart failure we give nesiritide. Why? Because it has diuretic action which will reduce the blood overload in cases of heart failure. It will reduce urine volume that will reduce pressure on heart. Now the next drug for cardiovascular system is actriparmel, nasal spray for PSVT.

[00:08:17]Now what is PSVT? PSVT is a type of arrhythmia which you call it as paroxysmal supraventricular tachycardia in which there is excessive activity of AV node. AV node fires on heart excessively. Hence in the treatment of PSVT, we give a drug AV node blockers. We give a drug AV node blockers and there are three AV node blocker ABC.

[00:08:49]A stands for adenosine. Adenosine is given IV and being an IV drug, it is given during an acute attack of PSVT.

[00:09:00]Then we have beta blocker. Beta blocker are given for long-term maintenance of PSVT because they are long-acting drug.

[00:09:09]But the point to be noted is that both adenosine and beta blocker are contraindicated in a patient of asthma because they can cause bronchoconstriction.

[00:09:20]So in cases of asthma, we give calcium channel blocker CCB verapamil. So verapamil is also given for maintenance of PSVT in asthmatic patient.

[00:09:35]Now the point is what about acute treatment? Don't you think a patient can take nasal spray during acute attack? So yes, we have a drug atri- pamil. So don't you think atri- pamil word is similar to verapamil? Pamil word is coming in both of them. So yes, atri- pamil is a calcium channel blocker just like verapamil and it can be given as a nasal spray for acute attack of PSVT. So which drug can be given in asthma during an acute attack? That is atri- pamil nasal spray just like calcium channel blocker verapamil, a fast acting drug.

[00:10:16]Next we have is aficamten and mavacamten.

[00:10:21]So you can see both drugs are ending with the word camten.

[00:10:25]Okay? And camten word is coming. These drugs are myosin inhibitor.

[00:10:34]They inhibit the action of myosin. If myosin and actin will not bind together, can we say the muscles of the heart will not contract? Because of this reason, it reduces cardiac contractility.

[00:10:49]And in which disease we want to reduce cardiac contractility? The disease is HOCM which stands for hypertrophic obstructive cardiomyopathy.

[00:11:03]Hypertrophic obstructive cardiomyopathy, we have to reduce the contractility of heart. The reason is very simple. In HOCM, there is excessive hypertrophy of ventricular muscle. And if you contract this ventricle excessively, there will be obstruction of blood flow to aorta.

[00:11:26]The blood will not go to the aorta. So increase in contractility will increase obstruction of the heart. So, that is why in HOCM, we have to reduce the contractility of heart. But, remember, HOCM, the first drug of choice to reduce contractility of heart is beta blockers. Beta blockers are the first drug of choice, and we know that beta blocker are contraindicated in asthma. So, in asthma, we give calcium channel blocker like verapamil as a second-line option for the treatment of HOCM. And after this, in refractory cases, or if the patient cannot tolerate verapamil or diltiazem, we give mavacamten or aficamten as a third-line option for the treatment of HOCM because they are myosin inhibitor. They will also reduce contractility of heart. Then, we have leero del si pep. Now, can we say this name? Leero means L word is coming.

[00:12:37]Then, del si pep word is coming, so we can write LDL word is coming. So, it decreases LDL cholesterol.

[00:12:46]Because it reduces LDL cholesterol, it is given for the treatment of hypercholesterolemia.

[00:12:54]So, what is the mechanism of action?

[00:12:56]Leero del si pep, it is a PCSK9 inhibitor. Now, what is PCSK9? In liver, we have LDL receptors. On liver, we have LDL receptors. Because of this LDL receptors, liver reuptake LDL from blood.

[00:13:16]Because of this reason, liver reduces blood LDL level. Now, in liver, we have an enzyme, PCSK9 enzyme, PCSK9 enzyme.

[00:13:27]This PCSK9 normally degrade LDL receptors from the liver. PCSK9 remove LDL receptors from the liver. Liver cannot reuptake LDL from the blood and the LDL level normally increases. So, if you inhibit PCSK9 enzyme, they will increase LDL receptors on liver.

[00:13:51]An increase in LDL receptors on liver will reduce blood LDL level. Now, what are the overall drugs we have for which are PCSK9 inhibitor? The first drug we have is evolocumab and alirocumab. Because map word are coming, these are the monoclonal antibody which inhibit PCSK9 enzyme. How we can remember? These monoclonal antibody will have LOC word in them. LOC means lowering of cholesterol. Lowering of cholesterol. Then we have another drug, inclisiran, very famous drug.

[00:14:31]Inclisiran, SI word is coming and RAN word is coming, that is siRNA.

[00:14:39]It is a silencing RNA which inhibits the production of PCSK9 protein. And leelo del cip It is a fusion protein. It is a fusion protein which inhibits PCSK9.

[00:14:56]Then we have fitusiran for hemophilia A and B. Now, again you can see SI RAN word is coming.

[00:15:05]So, again any drug having SI RAN word is there, we call this drug as silencing RNA.

[00:15:12]It is an silencing RNA which reduce the production of antithrombin.

[00:15:19]Remember, normally antithrombin inhibits thrombin. So, if you reduce the production of anti-thrombin, which molecule activity will increase?

[00:15:28]Obviously, thrombin activity will increase. And thrombin reduce bleeding in cases of hemophilia.

[00:15:37]So, fitusiran is a silencing RNA against anti-thrombin, which increase the activity of thrombin. Thrombin reduces bleeding in hemophilia. So, fitusiran.

[00:15:49]Next question. Or the next drug is depemokimab for asthma. Now, depemokimab, it's a monoclonal antibody that block interleukin 5 receptor.

[00:16:04]And in asthma, it is a depot injection.

[00:16:08]Depot means it is a very long-acting injection. Overall, now it is the longest-acting monoclonal antibody for asthma. That is depemokimab because it is a depot injection. How long it is acting? It is given once in 6 month for the prevention of asthma. Now, what are the other monoclonal antibody already approved in asthma? Similar to depemokimab, we have benralizumab. It also block interleukin 5 receptor.

[00:16:43]We have mepolizumab and reslizumab. It blocks interleukin 5 directly.

[00:16:49]So, it directly blocks interleukin 5, not the receptor of interleukin 5. And omalizumab, which block immunoglobulin E, it blocks IgE, which is located on the surface of mast cell, which causes release of mediators in cases of asthma.

[00:17:07]Now, let's talk about other allergic and inflammatory diseases of lungs or respiratory disease. We have benralizumab.

[00:17:16]So, catnip. Brenso catnip, it is given for BR for bronchiectasis.

[00:17:23]It is given for bronchiectasis. So, non that bronchiectasis which is not caused by cystic fibrosis.

[00:17:32]Now, bronchiectasis happens because of inflammation in lungs. Now, brenso catnip, it is a DPP-1 inhibitor. DPP stands for di peptidyl peptidase one inhibitor. Now, remember inflammatory molecules, they are peptides. They are degraded.

[00:17:55]Generally, they are inhibited by DPP.

[00:17:58]So, normally this DPP enzyme, it activates neutrophil serine protease which increases inflammation in lungs.

[00:18:08]Now, if you inhibit this DPP, can we say it will reduce inflammation in lung and which will inhibit the production or hampering of lungs? So, it will relieve bronchiectasis. So, DPP-1 inhibitor, it is an anti-inflammatory molecule. It reduces inflammation in bronchiectasis.

[00:18:30]Then, we have difalimast.

[00:18:33]Now, remember one rule, any drug which ends with the word "milast", any drug which ends with the word "milast" is a phosphodiesterase four inhibitor. So, it's a phosphodiesterase four inhibitor. So, difalimast, it is an anti-inflammatory molecule. So, if you inhibit phosphodiesterase enzyme, it reduces inflammation in the body. So, it reduces inflammation in cases of atopic dermatitis. Atopic dermatitis, D for difelikefast. It is given for some sort of dermatitis, that is atopic dermatitis, phosphodiesterase 4 inhibitor. Now, let's talk about other phosphodiesterase 4 inhibitor. They are also ending with the word "milast", you can see. Roflumilast, cilomilast, ibudilast. "ilast" word is coming. They reduce inflammation in the treatment of asthma and COPD.

[00:19:40]So, they are also anti-inflammatory molecule. Then, we have apremilast.

[00:19:45]Apremilast is given for the treatment of essential thrombocytosis.

[00:19:54]Essential thrombocytosis, increase in inflammation can lead to increased production of platelet. So, it will reduce platelet count, given in the treatment of thrombocytosis.

[00:20:06]Then, we have another milast, that is nérandomilast.

[00:20:11]So, because "milast" word is coming, it is a phosphodiesterase 4 inhibitor. It is given to decrease inflammation in cases of idiopathic pulmonary fibrosis, a new drug, nérandomilast. Now, remember in idiopathic pulmonary fibrosis, only three drugs are approved. How many drugs are approved for pulmonary fibrosis?

[00:20:39]That is only three drugs. The first drug for pulmonary fibrosis is nintedanib.

[00:20:46]Remember, any drug which ends with the word "nib" is a tyrosine kinase inhibitor.

[00:20:52]It's a tyrosine kinase inhibitor, which reduces fibrosis.

[00:20:57]Another drug we have is pirfenidone.

[00:21:01]P for pulmonary, inhibiting fibrosis. It It an antifibrotic drug. And the third drug which reduces fibrosis, a new drug, mirandolast, because inflammation leads to fibrosis.

[00:21:16]Only these three drugs are approved for the treatment of pulmonary fibrosis in PN.

[00:21:23]Then we have linerity linerixibat. Linerixibat, you can see I bet word is coming.

[00:21:32]So, it is a I bet inhibitor. It is a I bet inhibitor. I bet stands for ileal bile acid transporter. Now, remember if this bile is excreted from liver the bile is excreted into the liver and bile comes into the intestine. And approximately 95% of this bile again gets reabsorbed. 95% of the bile again gets reabsorbed. This is known as entero entero means intestine hepatic reabsorption of bile.

[00:22:11]Now, if bile gets excessively reabsorbed, bile deposits on skin and can lead to pruritus.

[00:22:19]So, deposition of bile is known as cholestatic pruritus and it happens in cases of primary biliary cholangitis.

[00:22:30]So, what we have to do, we have to inhibit reabsorption of bile in cases of cholestatic pruritus. And the first drug is line linerixibat.

[00:22:44]Linerixibat inhibits the reabsorption of bile by inhibiting I bet in transporter.

[00:22:52]Another drug and the only another drug approved for cholestatic pruritus in primary biliary cholangitis is cholestyramine. It's a older drug and it is considered to be the drug of choice for cholestatic pruritus. It is also a bile acid sequestrant. It increase the excretion of bile in feces.

[00:23:14]Cholestyramine increases in feces. So, in nutshell, we have to reduce bile level in our body in cases of cholestatic pruritus.

[00:23:24]Then we have now antibiotics or antimicrobial drug. So, we have two drug ending with the word -acin, -dacin or -acin. The first drug we have is zoliflodacin, zoliflodacin.

[00:23:40]And another drug we have is gepotidacin.

[00:23:44]So, any drug which ends with the word -dacin is topoisomerase inhibitor.

[00:23:51]Zoliflodacin inhibit topoisomerase two enzyme, which is also known as DNA gyrase B subunit. And gepotidacin inhibit topoisomerase four enzyme. It inhibit topoisomerase four enzyme. And zoliflodacin inhibit topoisomerase two enzyme. And these both drugs are given for the treatment of gonorrhea. Gonorrhea which is resistant to fluoroquinolones. Now, remember they are also similar to fluoroquinolone like ciprofloxacin, norfloxacin, but their binding subunit on topoisomerase enzyme is different. Fluoroquinolone also inhibit topoisomerase enzyme, but they act on different subunit. These drugs, they act on different subunit. That is why they can be given in fluoroquinolone resistant cases of gonorrhea, -dacin drugs are given. Then another antimicrobial, we have a vaccine for chikungunya virus.

[00:24:58]So, chikungunya the virus the vaccine is V for vaccine V Kounia. V Kounia is a vaccine against chikungunya virus the first vaccine. So, it uses some virus-like particle without any genetic material, without any RNA to stimulate antibody production. So, that is why because there is no genetic material, it will not lead to chikungunya infection, but it will stimulate antibody and it will produce antibody or immunity against this virus.

[00:25:31]So, right now it is approved for adults more than 12 years of age in three countries US, UK and Europe. Let's wait in other countries when it will get approved. Then another antimicrobial against a virus is clis rovimab. Clis rovimab R and V word is coming and S word is coming. So, it is a anti monoclonal antibody mab against RSV virus which stands for respiratory syncytial virus.

[00:26:05]So, it targets some fusion protein of RSV virus and hence it blocks the entry of RSV virus into human cell. So, remember RSV virus it can cause asthma-like illness which is known as bronchiolitis obliterans in premature neonate.

[00:26:24]So, it causes problem asthma-like illness in premature neonate. So, this monoclonal antibody is given in premature neonate. Apart from this new drug, the first monoclonal antibody against RSV virus was palivizumab. It was the first monoclonal antibody. Then we made nirsevimab and motavizumab motavimab. You can see all these monoclonal antibody are having VI word in them. VI means they are against virus. Now next we have is tradipitant.

[00:26:58]Tradipitant, remember any drug which ends with the word pitant is a neurokinin inhibitor. So it blocks neurokinin one receptor and it blocks neurokinin one receptor. It's a new drug for prevention of motion sickness. In motion sickness patient has vomiting when sitting in bus or car. Other drugs which are given for motion sicknesses scopolamine, diphenhydramine and promethazine. So they are anticholinergic or antihistaminic drugs.

[00:27:28]Then we have another drug ending with the word nitant, neurokinin antagonist, that is elinzanitant and fezolinetant.

[00:27:37]They are given for the treatment of postmenopausal hot flashes. Remember elinzanitant, it is a dual neurokinin one and three inhibitor, while fezolinetant is only neurokinin three inhibitor. Both are given for the treatment of hot flashes. Remember the overall drug of choice for the treatment of postmenopausal hot flashes is HRT, hormone replacement therapy. Replace the deficient hormone like estrogen and progesterone. In HRT resistant cases, we can give this nitant drug which are neurokinin blocker. Then we have another drug ecotrochindra. It is given for plaque psoriasis. It is the first oral drug which block interleukin three receptor for plaque psoriasis. One older drug we have is ustekinumab.

[00:28:29]kinumab. Ustekinumab is a monoclonal antibody which blocks interleukin 23, but it is given by injections. Then we have garadacimab.

[00:28:43]Donali don- donidalorsen and savvy try this chart. So you can pronounce this word. So these are very difficult to pronounce name also. So they are given for hereditary angioedema. So what happens in hereditary angioedema? There is increase in levels of bradykinin.

[00:29:03]Why? Because this bradykinin is produced from high molecular weight kininogen and kallikrein when they break down, bradykinin is produced and normally this is inhibited by C1 esterase enzyme. And if there is deficiency of C1 esterase enzyme, this step is not inhibited and there is increased production of bradykinin. So the overall drug of choice for hereditary angioneurotic edema is give this enzyme replacement from outside. You can give testosterone and danazol which can increase the production of this enzyme. We have lanadelumab ecallantide which inhibit kallikrein. We can give icatibant drug.

[00:29:46]Icatibant block the receptor of bradykinin that is B2 receptor. But now we have new drug. So the first is garadesimab.

[00:29:55]Garadesimab block clotting factor 12a which also inhibit kallikrein pathway. Clotting factor 12 leads to production of kininogen. Then we have donidalorsen which is an antisense oligonucleotide.

[00:30:12]Remember any drug ending with the word "orsen" is an RNA antisense.

[00:30:18]It also reduce the production of kallikrein. And the last drug we have is seby. And the last drug we have is sebytraelchart.

[00:30:26]Sebytraelchart is also kallikrein inhibitor. So these are the new drug. So try to remember C1 esterase inhibitor which is the overall drug of choice.

[00:30:36]Then we have certain drugs for eye disease like presbyopia, old age vision loss. So, we have aceclidine.

[00:30:44]Aceclidine is the only second drug approved for presbyopia. Apart from aceclidine, the overall drug of choice for presbyopia is pilocarpine. They are miotic drug. Both these drugs are cholinergic drug, which produce miosis.

[00:31:02]And miosis will lead to constriction of pupil, which will lead to pinhole effect, which will increase the depth and focus and improve near vision without causing myopic shift or nearsightedness. So, remember in presbyopia, we give miotic drug and improve near vision. So, the overall earliest approved drug is pilocarpine.

[00:31:26]And similar to pilocarpine, we have is aceclidine.

[00:31:30]Another eye disease drug we have is ecual trimon. Ecual trimon is given for dry eye disease. Dry eyes, can we call it as xerophthalmia?

[00:31:41]When there is a decrease in production of tears, the overall drug of choice for dry eyes is again pilocarpine.

[00:31:49]Because pilocarpine, apart from producing miosis, pilocarpine also causes lacrimation.

[00:31:56]And modification of pilocarpine is cevimeline. So, these drugs improve lacrimation, given for dry eye disease.

[00:32:04]But now we have a new drug, the third drug for dry dry eye disease is ecual trimon.

[00:32:11]Ecual trimon has a special mechanism of action. It acts on a receptor, TRMP8 receptor. TRMP stands for transient receptor potential melastatin. In physiology, you will learn this is a receptor which feels coolness or which will produce cooling sensation in your in your body. So, it's a cold sensing receptor. Now, because it's a cold sensing receptor, in case of dry eyes, it will produce cooling sensation, which will reduce the discomfort in eye. Plus, it also leads to production of natural tears, just like pilocarpine. So, last drug given for a cancer is immu- imlu- estrant, vep ti estrant. So, can we say all these drugs are ending with the word estrant?

[00:33:04]And what do you mean by estrant? ESTR stand for estrogen receptor.

[00:33:12]ANT stand for antagonist.

[00:33:15]So, any drug which ends with the word estrant block estrogen receptor. So, these drugs are known as SERD.

[00:33:24]And the first estrant or SERD, selective estrogen receptor downregulator, which was approved was fulvestrant. It was the first drug to be approved among SERD, which block estrogen receptor, EST antagonist. Then we made egalistrant, another estrant, and now we have made two more drug ending with the word estrant.

[00:33:49]All these drugs are given for the treatment of estrogen receptor positive breast cancer. Because estrogen receptor causes breast cancer, and normally the drug of choice for ER positive breast cancer is tamoxifen.

[00:34:07]So, these drugs are given in tamoxifen-resistant cases of breast cancer. What is tamoxifen? Tamoxifen is SERM, selective estrogen receptor modulator.

[00:34:21]That means on breast, it will block estrogen receptor. On some other organ, it will stimulate estrogen receptor. So, in tamoxifen-resistant cases, we rather give a drug SERD.

[00:34:33]They block estrogen receptor everywhere.

[00:34:36]They are more powerful drug SERD.

[00:34:40]So this is all about the new drugs approved in May 2025 to 2026. So you can follow these channels for more updates.

[00:34:49]Best wishes. Thank you very much.