#Small Drug molecules

[aragenlifesciences]

Fostering Scientific Excellence in Chemistry, Biology, and Development Services. Explore Aragen's Small Molecule APIs & Precision Formulations Expertise.

[angelnumber27]

Small Molecule Developed That Makes Immunotherapy Available to All Cancer Patients

[mestastop]

In the realm of cancer care, tackling metastasis treatment requires innovative approaches. At the forefront of this battle is the integration of cutting-edge technologies. Medical diagnosis using machine learning has emerged as a game-changer, enhancing our understanding of metastasis dynamics. Through meticulous research, our team at Mestastop is pioneering the application of this transformative technology (ReSULT) to decipher the intricacies of metastasis. Our vision extends beyond merely treating the primary tumor; we are committed to preventing metastasis through adjuvant interventions. With multiple drugs in the pipeline, we aim to revolutionize cancer care, synergizing early diagnostics and therapeutic modalities. Mestastop stands as a beacon of hope in the relentless pursuit of conquering metastasis. 

[luckydige45]

The global RNA targeting small molecule drug discovery market is valued at USD 1.43  Billion in 2023 and is projected to reach a value of USD 7.44 Billion by 2032 at a CAGR (Compound Annual Growth Rate) of 20.11% between 2023 and 2032

[laxmandige05]

The global small molecule drug discovery market size was exhibited at USD 75.98 billion in 2022 and is projected to hit around USD 163.58 billion by 2032, growing at a CAGR of 7.97% during the forecast period 2023 to 2032.

[industryupdate]

Psoriasis Drugs Industry Witnessed Fastest Growth in the APAC

The psoriasis drugs market will grow at a rate of 14% in the future and reach USD 53,210.6 million by 2030, as stated by a market report by P&S Intelligence. Get the sample pages of this report: https://bit.ly/3OXs87d The key factors accountable for the industry growth are quickly aging populace, increasing patient count suffering with psoriasis, increasing per capita income, escalating…

[reasonsforhope]

"People living with diabetes might have a new hope. Scientists have tested a new drug therapy in diabetic mice, and found that it boosted insulin-producing cells by 700% over three months, effectively reversing their disease.

Beta cells in the pancreas have the important job of producing insulin in response to blood sugar levels, but a hallmark of diabetes is that these cells are either destroyed or can’t produce enough insulin. The most common treatment is regular injections of insulin to manage blood sugar levels.

But a recent avenue of research has involved restoring the function of these beta cells. In some cases that’s started with stem cells being coaxed into new beta cells, which are then transplanted into patients with diabetes. Researchers behind this kind of work have described it as a “functional diabetes cure.”

Now, scientists at Mount Sinai and City of Hope have demonstrated a new breakthrough. Previous studies have mostly involved growing new beta cells in a lab dish, then transplanting them into mice or a small device in humans. But this new study has been able to grow the insulin-producing cells right there in the body, in a matter of months.

The therapy involved a combination of two drugs: one is harmine, a natural molecule found in certain plants, which works to inhibit an enzyme called DYRK1A found in beta cells. The second is a GLP1 receptor agonist. The latter is a class of diabetes drug that includes Ozempic, which is gaining attention lately for its side effect of weight loss.

The researchers tested the therapy in mouse models of type 1 and 2 diabetes. First they implanted a small amount of human beta cells into the mice, then treated them with harmine and GLP1 receptor agonists. Sure enough, the beta cells increased in number by 700% within three months of the treatment. The signs of the disease quickly reversed, and stayed that way even a month after stopping the treatment.

“This is the first time scientists have developed a drug treatment that is proven to increase adult human beta cell numbers in vivo,” said Dr. Adolfo Garcia-Ocaña, corresponding author of the study. “This research brings hope for the use of future regenerative therapies to potentially treat the hundreds of millions of people with diabetes.”

The results are intriguing, but of course being an animal study means there’s still much more work to be done before it could find clinical use. So far, harmine alone has recently undergone a phase 1 clinical trial in humans to test its safety and tolerability, while other DYRK1A inhibitors are planned for trials in humans next year.

Perhaps most importantly, the team will soon experiment with combining beta-cell-regenerating drugs with others that modulate the immune system. Ideally this should help overcome a major hurdle: the immune system will continue attacking new beta cells as they’re produced.

The research was published in the journal Science Translational Medicine."

-via New Atlas, July 14, 2024

[kdhhealthcomm]

Beating back cancer one small molecule at a time

Many of targeted therapies for cancer are small molecules created by the “drug hunters” of the pharmaceutical industry.

Targeted therapy revolutionizes outcomes for patients with cancer. Many of these targeted therapies are small molecules created by the “drug hunters” of the pharmaceutical industry. (1)  Drug hunters are looking for small molecules targeting cancer pathways. They examine protein-to-protein bonds, searching for and configuring small molecules that can fit into binding sites, like keys into locks.…

[mrunalnerkarblog]

Despite growth of biologic drugs, medicines based on small molecules remain important in the treatment of all types of diseases such as oncology disorders, infectious diseases, blood diseases, and cardiovascular diseases.

[prabha194]

Until 2027, the Small Molecule Drug Discovery market is expected to grow at a high rate

According to the latest study on “Small Molecule Drug Discovery Market Forecast to 2027– COVID-19 Impact and Global Analysis by Therapeutic Area, and Process/Phase,” the global small molecule drug discovery market was valued at US$ 24,976.14 million in 2019 and is projected to reach US$ 50,823.06 million by 2027; it is expected to grow at a CAGR of 9.5% during 2020–2027. The report highlights trends prevailing in the global small molecule drug discovery market and the factors driving market along with those that act as hindrances.

Small molecule drugs are used in targeted drug delivery in which small molecules pass through the cell membrane and acts on the specific cellular organelle or protein. The small molecule drugs are able to enter cells easily because of its low molecular weight. These molecules are better than monoclonal antibodies and other large molecule drugs due to their size, easy convertibility to oral form, and cost-effectiveness.

Based on process/phase, the global small molecule drug discovery market is segmented into target discovery, target validation, lead generation and refinement, and preclinical development. The lead generation and refinement segment held the largest share of the global small molecule drug discovery market in 2019. However, the target discovery is anticipated to register the highest CAGR during the forecast period. The target discovery segment is expected to grow owing to increasing demand of therapeutics, increasing product approvals, and rising investment in the drug discovery process.

Request for sample copy @ https://www.theinsightpartners.com/sample/TIPRE00004774/

Market leaders operating in the market have undertaken various organic growth strategies in the small molecule drug discovery Market. The small molecule drug discovery market majorly consists of the players such as Pfizer Inc., Bristol-Myers Squibb Company, Merck KGaA, GlaxoSmithKline Plc, AstraZeneca, Johnson & Johnson Services, Inc., TEVA PHARMACEUTICAL INDUSTRIES LTD, Boehringer Ingelheim International GmbH, and Allergan Plc. The companies have been implementing various strategies that have helped the growth of the company and in turn have brought about various changes in the market. The companies have utilized organic strategies such as launches, expansion, and product approvals. Moreover, the companies have utilized inorganic strategies including mergers & acquisitions, partnership, and collaborations.

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Contact Us: Contact Person: Sameer Joshi  Phone: +1-646-491-9876

[phoenixblair666]

It Only Takes One Second: A Logan Howlett X Fem!Reader Story

This story takes place in the X-Men trilogy. It's a romance between Logan and Fem!Reader, where the reader goes through a traumatic experience that allows her mutant powers to emerge. She goes to Xavier's school in search of sanctuary but finds Logan instead. When He helps her learn how to use and control her powers, he creates a valuable new member of the X-Men, but what started as helping a new recruit find their footing, turns into a blossoming romance.

Authors Note: This story will be in multiple parts. As of now how many parts, is to be determined. The story starts off slow, but additional parts will be added. Enjoy! ˗ˋˏ ♡ ˎˊ˗

Word Count: 1,207

Reading Time Approximately: 5 Minutes

WARNINGS: Mentions of Traumatic experiences (Car crash), Mentions of Anxiety, Mentions of Hospitalization

(Part: 1) How It All Started

˚₊ ˚ ‧₊ .:･˚₊ ˚ ‧₊ .:･˚₊ *˚˚₊ ˚ ‧₊ .:･˚₊ ˚ ‧₊ .:･˚₊ *˚ ˚₊ ˚ ‧₊ .:･˚₊ ˚ ‧₊ .

Driving has always given you a sense of peace. That certain feeling of highway hypnosis was more than welcomed; the cool breeze in your hair, the gentle warmth from the sun shining through your windshield, and classic tunes fit for a twenty-three-year-old woman playing through your out-of-date stereo.

You never feared the long roads during these trips, nor did you fear where they would take you. Living in a van had its perks. One day you may want to lie beachside, lemonade in hand, the next you're driving through the Rocky Mountains, taking in the natural sights. Today that feeling changed.

Screeching tires echoed through the twined peaks on either side of you, the smell of burnt rubber filling your vehicle. You tried to take control of the wheel as best you could, but the invisible ice covering the pavement made it incredibly difficult. Your car swerved one way, then the next before the sound of metal against metal was heard, airbags deploying, scraping your face, leaving first-degree burns against your skin. Now you were airborne, freefalling off the side of a mountain. Time feels as if it slows as you watch the raging river below get closer and closer with each second.

Then it happens. Suddenly your body senses the air surrounding you. The way the gaseous molecules float freely, only parting ways when they touch your solid form. You can feel the vibrations from each of these molecules not on your skin but deep within your muscles, a sensation that is completely foreign to you.

The car is only a few yards away from crashing into the aggressive waters when your body begins to use the surrounding air as leverage, and you begin to float on your own accord. It's not gravity lifting you from your seat, but it's you, manipulating the natural resource. Everything happens too quickly for this newfound ability to be of use, and before you know it your car is making an impact with the water. The surface of the river is like concrete against the metal, crushing the hood to your knees. Your windshield shatters, allowing water to flood the interior of the vehicle, and then everything goes black.

══════════════════════════════

The smell of rubbing alcohol and soap is the first thing your senses pick up, then the constant beeping in your ears. Your fingers feel the rough texture of fabric as you weakly grip a set of white sheets. All of your senses slowly come back, one by one, acclimating you to your surroundings. Finally, your eyes flutter open. Your vision is blurry, but you can see the bright fluorescent lights shining down on you. You blink hard, trying to make the rest of the room visible, succeeding when you begin to notice the objects around you. A countertop with a sink, an empty armchair, medical posters, and IVs wrapping around your arm with a small needle filling your body with a plethora of drugs.

Just like the rest of your senses, the unfamiliar buzzing in your muscles returns. Once again, you feel the sheer power of the surrounding air in your body. This is a sensation that is completely new to you, it is frightening. Your heart begins to quicken, and the machine next to you detects the rapid pulse, alerting nearby nurses. You begin to paw at the IVs that adorn your arm, ripping the needle from your skin and discarding it on the floor, allowing liquid to pool on the clean white tiles. Your body begins to hover as you panic, lifting a few feet above the bed. A nurse opens the curtain that led into your room, gasping at the sight before him.

As you float, the feeling of uncertainty washes over you. Everything that was happening to you in this moment was unnatural, almost alien. The fact that you survived the horrible crash the day before, and now you can fly without trying, was some sort of strange miracle.

Nothing in your life has been or will be the same since this day.

══════════════════════════════

The sign against the brick wall was a clear indicator that you had reached your destination. You had heard from one of the doctors a few weeks ago that there was a place for 'You people' that acted as a sanctuary. Until then you had heard few stories of mutants, let alone seen one for yourself. And now here you are, standing at the entrance of Xavier's School for Gifted Youngsters. You inhale sharply, feeling a ball sit in your chest, all worries flooding your mind at once.

Hesitantly you take one heavy step forward, then the next. Gravel crunches under your combat boots as you make your way to the large mansion-turned-school. Two large oak doors decorate the front of the classic old building, and an elegant porch covers them, while vines grow upwards against the brick, some even covering the many windows that adorn the structure. A large water fountain sits in the middle of a rounded driveway, and different types of foliage surround the man-made body of water.

What was once gravel turns into a stone path, leading to the driveway. Your steps become more wary as you approach the stairs of the porch. The unknown sits behind the oak barriers, making your heartbeat thump against your ribcage. A few more steps and you are right in front of said barrier. Lifting your arm had proven to be more difficult than expected as thoughts raced through your skull. Despite this, the rough skin against your knuckles meets the solid object with three small knocks.

Your anxiety spikes as you wait for someone to answer. You almost don't notice that you're holding your breath, barely able to remind yourself to keep breathing. One of the doors swings open, making you jump at the abrupt motion. A tall man peers down at your shorter self, eyeing you intently. His hair is pitch black and came to two catlike peaks at the top, with facial hair that hugs his jaw but stopped above his lip and chin, leaving only a small amount of stubble. His eyes are a light hazel color, resembling two rounded drops of honey and his body is quite built. He wore a white, wife-pleaser that showed every muscle under his lightly tanned skin, along with a dark blue, denim pair of jeans.

Your breath hitches in your throat, as your eyes meet his. The stare lasts longer than you'd like, but when his hardened expression turns curious, you find it easier to find your voice. "Is this Xavier's School for the Gifted?" You ask sheepishly, searching his eyes for a silent response. The man looks you up and down, then to the gate that you had entered from. Once his eyes meet yours again, he smirks. "Do you know how to read?" He questions, lifting an eyebrow. You nod quickly, feeling quite small at the hands of his satirical response. His features change for a third time, and he smiles. "Then I think you're at the right place."

˚₊ ˚ ‧₊ .:･˚₊ ˚ ‧₊ .:･˚₊ *˚˚₊ ˚ ‧₊ .:･˚₊ ˚ ‧₊ .:･˚₊ *˚˚₊ ˚ ‧₊ .:･˚₊ ˚ ‧₊ .:

You try to match his smile, but it comes off as nervous. He chuckles at your shy exterior before opening the door further and allowing you entrance.

Part 2: Nightmares

[aragenlifesciences]

Small molecule Drug discovery companies

Leading the way in pharmaceutical innovations, CDMO pharma companies like Aragen excel in providing comprehensive services. As premier Small molecule Drug discovery companies, they drive the development of groundbreaking therapies, ensuring seamless integration from concept to commercialization.

[excalculus]

I saw some mentions of rabies going around again and have no clue what's set it off this time, but given recent scientific developments I want to revisit the idea of curing symptomatic rabies.

First things first: there is still no practical way to do this. The famous Milwaukee Protocol fails far more frequently than it succeeds, and even the successes are not making it out in anything like a normal state. It's been argued that it should no longer be considered a valid treatment [1] due to these issues; any continued use is because there's literally nothing else on the table.

However. There are now two separate studies showing it's possible to cure rabies in mice after the onset of symptoms. The lengths you have to go to in order to pull this off are drastic, to put it mildly, and couldn't really be adapted to humans even if you wanted to. But proof of concept is now on the board.

long post under the cut, warnings for animal experimentation and animal death. full bibliography at the end and first mention of each source links to paper.

Quick recap - rabies is a viral disease of mammals usually transmitted through the saliva of an infected animal. From a contaminated bite wound, it propagates slowly for anywhere from days to months until it reaches the central nervous system (CNS). Post-exposure vaccination can head it off during this phase, but once it reaches the CNS and neurological symptoms appear it's game over. There will typically be a prodromal phase where the animal doesn't act right - out at the wrong time of day, disoriented, abnormally friendly, etc. This will then progress to the furious (stereotypical "mad dog" disease) and/or paralytic phases, with death eventually caused by either seizures or paralysis of the muscles needed for breathing.

That's the course we're familiar with in larger animals. Mice, though, are fragile little creatures with fast metabolisms.

In the first study's rabies infection model, lab mice show rabies virus in the spinal cord by day 4 after infection and in the brain by day 5. Weight loss and slower movement start by day 7, paralysis starting from the hind limbs from day 8 on, and if not euthanized first they're dead by day 10-13. [2]

This study (fittingly conducted at the Institut Pasteur) had two human monoclonal antibodies, and wanted to see if there was any possibility they could be used to cure rabies after what we think of as the point of no return.

Injecting the antibodies into muscle saved some mice if done at days 2 or 4, and none if done later, even at high doses of 20 milligrams per kilogram of body weight of each. Conclusion: targeting the virus out in the rest of the body is no use if it's already replicating in the CNS.

Getting a drug past the blood-brain barrier is, to use a highly technical term, really fucking hard. It's the sort of problem that even the best-funded labs and biggest companies in the world routinely fail at. And that's for small molecule drugs, which are puny compared to antibodies.

But this isn't drug development for a clinical trial. This is a very, very early proof-of-concept attempt, which means you're willing to ignore practicality to see if this idea is even remotely workable. So you can do things like brute force the issue by cutting through the skull to implant a microinfusion pump, which lets you deliver the antibodies directly into the normally-protected space around the brain. Combine this with the normal injections, and you can treat both the CNS and the rest of the body at the same time. Here's a survival graph of treated mice. X axis is days, Y axis is percentage of mice in that group still alive.

Figure 2A from reference 2, accessed February 2024

The fact that the blue, green, and purple lines did anything other than sink horribly to zero is unheard of. When the combination treatment was started at day 6, 100% of the mice survived. Started at day 7 (prodromal phase), 5 out of 9 mice recovered and survived. Started at day 8 (solidly symptomatic, paralysis already starting to set in), 5 of 15 mice recovered and survived. And when they say "survived", they kept these mice all the way to day 100 to make sure. Some of them had permanent minor paralysis but largely they were back to being normal mice doing normal mouse things. So, success, but by pretty extreme means.

Enter the second paper [3]. This was a different approach using a single human monoclonal antibody against Australian bat lyssavirus (ABLV - closely related to rabies, similar symptoms in humans) to try for a cure without needing to deliver treatments directly into the CNS. They also made a luminescent version of ABLV that let them directly image viral activity, so they could see both where the virus was replicating and how much there was in a live mouse.

Figure 1 from reference 3, accessed February 2024

Mice infected with ABLV start showing symptoms around day 8. You can see in the figure that at day 3 there's viral replication in the foot at the site of infection, which has shifted into the spine and brain by day 10. So what happens if you give one of these doomed mice one single injection of the antibody into the body?

Done at day 3, the virus doesn't make it to the brain until day 14, and while disease does set in after that around 30% of the mice survive. Days 5 and 7 are much more interesting. Those mice still develop symptoms at day 8, but the imaging shows the amount of virus in their spines and brains never gets anywhere near the levels seen in untreated controls, and within days it starts to decrease. Around 80% of day 5 and 100% of day 7 mice survive.

Okay, sure, you can stop another lyssavirus, but technically you did start treatment before symptoms appeared. What about symptomatic rabies?

The rodent-adapted rabies strain CVS-11 starts causing symptoms as early as day 3 after infection, and untreated mice die between days 8 and 11. The same single dose of antibody saved 67% of mice treated on day 5 and 50% of mice treated on day 7. Without making the luminescent version of the virus there's no real-time imaging of the infection, but you can still track symptoms.

Figure 2 from reference 3, accessed February 2024. CVS-11 is the name of the rodent rabies strain and F11 is the name of the antibody.

Disease score is a combination of several metrics including things like whether the mice are behaving normally and whether they show signs of paralysis. In untreated mice it goes up and up, and then they die. If one of those lines starts coming back down and continues past day 10 or so, that's a mouse that recovered. The success rate isn't as good as against ABLV, but again, this is a rabies strain specifically adapted to rodents and treatment wasn't started until it was well-established in the CNS.

So how on earth is this happening? The antibody neutralizes both ABLV and rabies really well in a test tube, but we've already established that there's no way a huge lumbering antibody is making it past the blood-brain barrier without serious help. Something about the immune response is clearly making it in there though. And it turns out that if you start trying this cure in mice missing various parts of their immune systems, mice without CD4+ T cells don't survive even with the treatment. By contrast mice without CD8+ T cells take longer to work through the infection, but they eventually manage it and are immune to reinfection afterwards.

To grossly oversimplify the immune system here, CD4+ are mature helper T cells, which work mostly by activating other immune cells like macrophages (white blood cells) and CD8+ T cells (killer T cells) against a threat.

Normally, T cells are also kept out by the blood-brain barrier, but we know that in certain specific cases including viral infection they can pass it to migrate into the brain. In the brains of the infected mice for which antibody treatment either wasn't given or didn't work, you can find a roughly even mix of CD8+ and CD4+ T cells along with a whole lot of viral RNA. But in the brains of those successfully fighting off the infection, there's less viral RNA and the cells are almost exclusively CD4+. So the antibody doesn't work by neutralizing the virus directly - something about it is activating the animal's own immune system in a way that gives it a fighting chance.

Again, neither of these proof of concept treatments is really workable yet as a real world cure. The first one is almost hilariously overkill and still has a pretty good chance of failure. The second is less invasive but careful sequencing still shows both low-level viral replication and signs of immune response in the brains of the survivors even at day 139, so it may not be truly clearing the virus so much as trading a death sentence for life with a low-level chronic infection. But now we know that 1. curing rabies after symptoms begin is at least theoretically possible, and 2. we have some clues as to mechanisms to investigate further.

Not today. Not tomorrow. But maybe not never, either.

References:

Zeiler, F. A., & Jackson, A. C. (2016). Critical appraisal of the Milwaukee protocol for rabies: this failed approach should be abandoned. Canadian Journal of Neurological Sciences, 43(1), 44-51.

de Melo, G. D., Sonthonnax, F., Lepousez, G., Jouvion, G., Minola, A., Zatta, F., ... & Bourhy, H. (2020). A combination of two human monoclonal antibodies cures symptomatic rabies. EMBO molecular medicine, 12(11), e12628.

Mastraccio, K. E., Huaman, C., Coggins, S. A. A., Clouse, C., Rader, M., Yan, L., ... & Schaefer, B. C. (2023). mAb therapy controls CNS‐resident lyssavirus infection via a CD4 T cell‐dependent mechanism. EMBO Molecular Medicine, 15(10), e16394.

[mestastop]

Discover groundbreaking advancements in treatment for distant metastasis that are revolutionizing cancer care. Addressing the challenges of metastasis requires innovative approaches, and our team at Mestastop is at the forefront. Leveraging cutting-edge technology like ReSULT, we not only focus on understanding cancer metastasis but also empower early diagnosis.

[mindblowingscience]

MIT chemists have developed a new way to synthesize complex molecules that were originally isolated from plants and could hold potential as antibiotics, analgesics, or cancer drugs. These compounds, known as oligocyclotryptamines, consist of multiple tricyclic substructures called cyclotryptamine, fused together by carbon–carbon bonds. Only small quantities of these compounds are naturally available, and synthesizing them in the lab has proven difficult. The MIT team came up with a way to add tryptamine-derived components to a molecule one at a time, in a way that allows the researchers to precisely assemble the rings and control the 3D orientation of each component as well as the final product.

Continue Reading.

[science-lover33]

Exploring the Marvels of Biological Macromolecules: The Molecular Machinery of Life (Part 3)

Proteins and Enzymes: Catalysts of Molecular Reactions

Proteins are the central players in macromolecular interactions. Enzymes, a specialized class of proteins, catalyze biochemical reactions with remarkable specificity. They bind to substrates, facilitate reactions, and release products, ensuring that cellular processes occur with precision.

Protein-Protein Interactions: Orchestrating Cellular Functions

Proteins often interact with other proteins to form dynamic complexes. These interactions are pivotal in processes such as signal transduction, where cascades of protein-protein interactions transmit signals within cells, regulating diverse functions such as growth, metabolism, and immune responses.

Protein-Ligand Interactions: Molecular Recognition

Proteins can also interact with small molecules called ligands. Receptor proteins, for instance, bind to ligands such as hormones, neurotransmitters, or drugs, initiating cellular responses. These interactions rely on specific binding sites and molecular recognition.

Protein-DNA Interactions: Controlling Genetic Information

Transcription factors, a class of proteins, interact with DNA to regulate gene expression. They bind to specific DNA sequences, promoting or inhibiting transcription, thereby controlling RNA and protein synthesis.

Membrane Proteins: Regulating Cellular Transport

Integral membrane proteins participate in macromolecular interactions by regulating the transport of ions and molecules across cell membranes. Transport proteins, ion channels, and pumps interact precisely to maintain cellular homeostasis.

Cooperativity and Allosteric Regulation: Fine-Tuning Cellular Processes

Cooperativity and allosteric regulation are mechanisms that modulate protein function. In cooperativity, binding one ligand to a protein influences the binding of subsequent ligands, often amplifying the response. Allosteric regulation occurs when a molecule binds to a site other than the active site, altering the protein's conformation and activity.

Interactions in Signaling Pathways: Cellular Communication

Signal transduction pathways rely on cascades of macromolecular interactions to transmit extracellular signals into cellular responses. Kinases and phosphatases, enzymes that add or remove phosphate groups, play pivotal roles in these pathways.

Protein Folding and Misfolding: Disease Implications

Proteins must fold into specific three-dimensional shapes to function correctly. Misfolded proteins can lead to Alzheimer's, Parkinson's, and prion diseases. Chaperone proteins assist in proper protein folding and prevent aggregation.

References

Voet, D., Voet, J. G., & Pratt, C. W. (2016). Fundamentals of Biochemistry: Life at the Molecular Level. Wiley.

Lehninger, A. L., Nelson, D. L., & Cox, M. M. (2017). Lehninger Principles of Biochemistry. W. H. Freeman.

Berg, J. M., Tymoczko, J. L., & Stryer, L. (2002). Biochemistry. W. H. Freeman