Comment Some estimates (Score 5, Interesting) 25
As is too often the case, the article is paywalled, and crucial information allowing for real understanding is hidden.
But, based on info given, some back-of-the-napkin calculations can be done. These are done with the intent to estimate doses, and thereby answer questions brought up in some of the comments here.
One obvious detail is that this will be intravenous infusion, something that can be started in the field with emt's and paramedics, or expeditiously in the ER.
Basics - CO poisoning is common, from vehicle and marine exhaust, faulty lamps-furnaces-camping equipment, faulty home heating, house fires, et al. Normally, hemoglobin (hgb) shuttles oxygen around. Hemoglobin is protein red blood cells, each hemoglobin protein carrying four heme groups each holding one iron atom. That iron atom wants to "rust" and bind with oxygen. Oxygen is picked up by hgb as blood goes through the lungs. In the periphery where O2 is needed, local chemistry based on CO2 and acid-base levels allow hgb to release the oxygen. It is one of nature's brilliant systems, and key is that Hgb can easily bind and unbind.
But, CO has very high affinity for hemoglobin, and once iron bound, it blocks oxygen binding. Once locked in, it does not dislodge, so the body loses that oxygen carrying capacity. All red cells eventually die and are replaced, so the situation is self correcting for low levels of carboxyhemoglobin, as you might have after sitting around a campfire or commonly in smokers. Generally, up to 10% carboxyhemoglobin is tolerated with no or minimum symptoms. On the other hand, 50% carboxyhemoglobin (instead of hemoglobin or oxyhemoglobin) is highly toxic and needs icu care, often fatal, and 70% COHg is uniformly fatal. Anything that can dislodge CO and thereby bring current red cells back "on line" is the goal.
Current best rx is oxygen, hyperbaric oxygen, and blood replacement in more extreme case, but these all take time to implement. This new RcoM peptide sounds promising for very rapid effects, in minutes.
Now, here is the estimated stoichiometry:
There is published info about RcoM which is a peptide with about 250 residues (amino acids), and this paper intro implies they modified the natural protein, presumably making a smaller peptide having the same CO binding affinity.
Each red cell has about 250 million hgb molecules, meaning 1 billion iron atoms = 10^9.
Red blood cell (rbc) counts in normal healthy people are about 5 million cells per cubic mm = 5 x 10^6.
A liter has one million cubic mm per liter = 10^6.
Normal adult blood volume is about 5 liters.
So : (10^9 iron atoms per rbc) x (5 x 10^6 rbc / cu.mm) x (10^6 cu.mm / liter) x (5 liters)
= 25 x 10^21 = 2.5 x 10^22, round off to 10^22 iron atoms per circulating blood (other rbc's are sequestered in bone marrow and spleen, but we can ignore for this calculation).
Avogadro's number is about 6 x 10^23. Rounding off :
(10^22 iron atoms / blood volume) / (10^23 atoms / mole) = 10^-1 moles/ blood volume.
In CO poisoning, each iron binds on CO, so there is 1:1 molar equivalency.
What I can infer from the article stub is that the RcoM peptide they made has high and tight CO binding, and once joined, the complex is excreted by the kidneys. It also sounds like one peptide of RcoM binds one molecule CO, so the molar stoichiometry is 1:1.
That means that 0.1 moles of their RcoM-HBD is need to suck up 0.1 moles of CO. That would be needed in a patient who has 100% carboxyhemoglobin, but they would be dead already, so we are talking about 0.05 moles for someone with 50% COHg.
Next question is - how many grams is 1 mole of RcoM-HBD?
The kidney is a giant filter. Pressurized blood in renal capillaries (going through a structure called the glomerulus) is filtered through a membrane into the urine space. Small molecules are forced across the membrane - water, electrolytes (inorganics), and small organics. The downstream renal tubules reabsorb the water and ash as they cannot otherwise be conserved (new such molecules must come from diet). Small organics are mainly waste that needed to be eliminated, or some small bioactive chemicals that the body easily regenerates. The healthy kidney has such a fine mesh "sieve" that larger molecules like proteins cannot pass through. Proteinuria is a key marker of renal disease as the membrane gets too porous. However, some peptides, too small to be officially classified as proteins, can get through. What is the limit on size of chemicals that normally get through the sieve or are blocked?
Peptides 10-12 kDa (kilodaltons, molecular weight units) filter freely. Proteins 50-70 kDA are blocked. In between, filtration drops off according to some curve. It is safe to assume from the paper that RcoM-HBD, freely and easily eliminated in the urine, is down there around 10-12 kDa.
How many residues (individual chained AA amino acids) are in a peptide weighing 10,000 - 12,000 daltons?
Average amino acid weight is about 110 da. So, (11,000 DA per RcoM-HBD) / (110 Da per AA) = 100 aa's.
Native RcoM has about 250 residues, so RcoM-HBD / RcoM = 100 / 250 = 0.4 which is also the relative molecular weight.
That number is not needed for further calculations, but it implies that these guys re-engineered RcoM to eliminate 60% of its weight, and that sounds quite plausible trying to derive a pharmaceutical from a natural source.
So -
In a patient with 50% COHg, we need 0.05 moles of therapeutic RcoM-HBD.
Molar weight is the molecular weight in grams, so if RcoM-HBD has molar weight 11,000, then
(11,000 gm / mole) x (0.05 moles) = 550 GM.
And - believe it or not, that is a reasonable number.
An analogous drug (in terms of bulk biological chemistry) is mannitol, a 6-carbon polyol (a sugar alcohol, basically a sugar molecule that stays straight instead of chasing its tail into a ring). It is a vital drug for treating brain edema, pulmonary edema, renal failure, trauma resuscitation, etc. Depending on the clinical situation, it is given IV "push", or IV drip, or both, push then drip. Push doses are typically 25-100 Gm.
So, a drug like this could plausibly given as, let's say, 50 Gm at once, then a continuous drip until a total of 550 Gm is administered. A comparable dose, 50 Gm, maybe every 10-15 minutes, would see a full course of rx administered in 2-3 hours.
Depending on the pharmacokinetics and clinical pharmacy, which would have to be studied in detail for approval and clinical use, might reveal higher lower limits or tolerances, and actual care adjusted accordingly.
I can foresee something like this being combined with mannitol infusion perhaps, to augment renal blood flow and glomerular clearance (if the RcoM is not inherently osmotic, probably not at 11 kDA), plus short term 100% oxygen but only for 2-3 hours until CO is cleared enough.
This stuff is pretty brilliant, and important, and life saving. Many of these estimates might be right or wrong, and many of these details might already be worked out by them - but behind a paywall - you all know about that.
But this "Fermi problem" estimation comes up with clinically and biologically realistic numbers.